Review



human aml cell lines u937  (DSMZ)


Bioz Verified Symbol DSMZ is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 96
      Buy from Supplier

    Structured Review

    DSMZ human aml cell lines u937
    A) Overall survival analysis of <t>AML</t> patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in <t>AML</t> <t>cell</t> lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, <t>U937,</t> and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Human Aml Cell Lines U937, supplied by DSMZ, used in various techniques. Bioz Stars score: 96/100, based on 566 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human aml cell lines u937/product/DSMZ
    Average 96 stars, based on 566 article reviews
    human aml cell lines u937 - by Bioz Stars, 2026-03
    96/100 stars

    Images

    1) Product Images from "CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins"

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    Journal: bioRxiv

    doi: 10.64898/2025.12.24.696284

    A) Overall survival analysis of AML patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in AML cell lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, U937, and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Figure Legend Snippet: A) Overall survival analysis of AML patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in AML cell lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, U937, and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.

    Techniques Used: Expressing, MANN-WHITNEY, Mutagenesis, Activity Assay, Gene Expression, CRISPR, Control, Quantitative RT-PCR, Flow Cytometry, Phospho-proteomics, Western Blot

    A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations of CX-4945 and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).
    Figure Legend Snippet: A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations of CX-4945 and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).

    Techniques Used: Activity Assay, Staining, Flow Cytometry, Expressing

    A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.
    Figure Legend Snippet: A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.

    Techniques Used: Western Blot, Quantitative RT-PCR, Control

    A) Principal component analysis (PCA) plot showing the distribution of Molm-13 (parental) versus Molm-13/VR (with and without drug treatment for 24h) AML cell lines (n=2 out of three replicates). B) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in Molm-13 and Molm-13/VR AML cell lines transcriptome. C-D) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘B’ ( C ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( D ). E) Gene-Concept network analysis depicting the gene-to-gene interconnection in the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented with significant differentially expressed genes in Molm-13/VR cells with CX+VEN combo treatment (control vs. Combo). Node size refers to the number of genes in the enriched pathway. Genes shared between edges refer to terms belonging to multiple pathophysiological categories. F) Principal component analysis (PCA) plot showing the distribution of PDX 2016-7 (with and without drug treatment for 24h) AML cells (n=3). G) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in PDX 2016-7 AML cells transcriptome. H-I) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘G’ ( H ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( I ). J) Heatmap showing the expression profile of genes highly expressed in VEN non-responders (adapted from ), p53 target genes, and BCL2-family members (anti-apoptotic and pro-apoptotic) in PDX 2016-7 cells.
    Figure Legend Snippet: A) Principal component analysis (PCA) plot showing the distribution of Molm-13 (parental) versus Molm-13/VR (with and without drug treatment for 24h) AML cell lines (n=2 out of three replicates). B) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in Molm-13 and Molm-13/VR AML cell lines transcriptome. C-D) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘B’ ( C ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( D ). E) Gene-Concept network analysis depicting the gene-to-gene interconnection in the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented with significant differentially expressed genes in Molm-13/VR cells with CX+VEN combo treatment (control vs. Combo). Node size refers to the number of genes in the enriched pathway. Genes shared between edges refer to terms belonging to multiple pathophysiological categories. F) Principal component analysis (PCA) plot showing the distribution of PDX 2016-7 (with and without drug treatment for 24h) AML cells (n=3). G) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in PDX 2016-7 AML cells transcriptome. H-I) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘G’ ( H ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( I ). J) Heatmap showing the expression profile of genes highly expressed in VEN non-responders (adapted from ), p53 target genes, and BCL2-family members (anti-apoptotic and pro-apoptotic) in PDX 2016-7 cells.

    Techniques Used: Functional Assay, Control, Expressing

    A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.
    Figure Legend Snippet: A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.

    Techniques Used: Derivative Assay, Irradiation, Injection, Transplantation Assay, Flow Cytometry, Western Blot



    Similar Products

    aml cell lines  (ATCC)
    99
    ATCC aml cell lines
    Downregulation of TERF2 suppresses <t>AML</t> cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or <t>TERF2-knockdown</t> <t>MOLM13</t> cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.
    Aml Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aml cell lines/product/ATCC
    Average 99 stars, based on 1 article reviews
    aml cell lines - by Bioz Stars, 2026-03
    99/100 stars
    		  Buy from Supplier
    human aml cell lines u937  (DSMZ)
    96
    DSMZ human aml cell lines u937
    A) Overall survival analysis of <t>AML</t> patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in <t>AML</t> <t>cell</t> lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, <t>U937,</t> and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Human Aml Cell Lines U937, supplied by DSMZ, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human aml cell lines u937/product/DSMZ
    Average 96 stars, based on 1 article reviews
    human aml cell lines u937 - by Bioz Stars, 2026-03
    96/100 stars
    		  Buy from Supplier
    human aml cell lines u937  (ATCC)
    99
    ATCC human aml cell lines u937
    A) Overall survival analysis of <t>AML</t> patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in <t>AML</t> <t>cell</t> lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, <t>U937,</t> and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Human Aml Cell Lines U937, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human aml cell lines u937/product/ATCC
    Average 99 stars, based on 1 article reviews
    human aml cell lines u937 - by Bioz Stars, 2026-03
    99/100 stars
    		  Buy from Supplier
    aml cell lines  (DSMZ)
    96
    DSMZ aml cell lines
    A) Overall survival analysis of <t>AML</t> patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in <t>AML</t> <t>cell</t> lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, <t>U937,</t> and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Aml Cell Lines, supplied by DSMZ, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aml cell lines/product/DSMZ
    Average 96 stars, based on 1 article reviews
    aml cell lines - by Bioz Stars, 2026-03
    96/100 stars
    		  Buy from Supplier
    human aml cell line molm13  (DSMZ)
    96
    DSMZ human aml cell line molm13
    A) Overall survival analysis of <t>AML</t> patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in <t>AML</t> <t>cell</t> lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, <t>U937,</t> and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Human Aml Cell Line Molm13, supplied by DSMZ, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human aml cell line molm13/product/DSMZ
    Average 96 stars, based on 1 article reviews
    human aml cell line molm13 - by Bioz Stars, 2026-03
    96/100 stars
    		  Buy from Supplier
    aml cell line sig m5  (DSMZ)
    93
    DSMZ aml cell line sig m5
    A) Overall survival analysis of <t>AML</t> patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in <t>AML</t> <t>cell</t> lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, <t>U937,</t> and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Aml Cell Line Sig M5, supplied by DSMZ, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aml cell line sig m5/product/DSMZ
    Average 93 stars, based on 1 article reviews
    aml cell line sig m5 - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier
    aml cell lines thp1  (DSMZ)
    96
    DSMZ aml cell lines thp1
    A) Overall survival analysis of <t>AML</t> patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in <t>AML</t> <t>cell</t> lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, <t>U937,</t> and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Aml Cell Lines Thp1, supplied by DSMZ, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aml cell lines thp1/product/DSMZ
    Average 96 stars, based on 1 article reviews
    aml cell lines thp1 - by Bioz Stars, 2026-03
    96/100 stars
    		  Buy from Supplier
    aml 12 cell line  (ATCC)
    99
    ATCC aml 12 cell line
    A) Overall survival analysis of <t>AML</t> patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in <t>AML</t> <t>cell</t> lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, <t>U937,</t> and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.
    Aml 12 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/aml 12 cell line/product/ATCC
    Average 99 stars, based on 1 article reviews
    aml 12 cell line - by Bioz Stars, 2026-03
    99/100 stars
    		  Buy from Supplier

    Image Search Results


    Downregulation of TERF2 suppresses AML cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: Downregulation of TERF2 suppresses AML cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.

    Article Snippet: AML cell lines (MOLM13 and THP-1) were obtained from the American Type Culture Collection (ATCC) and were cultured in RPMI-1640 medium (Gibco, Grand Island, USA) containing 10% heat-inactivated fetal bovine serum (FBS; Gibco) under standard conditions (37 °C, 5% CO 2 ).

    Techniques: Quantitative RT-PCR, Knockdown, Western Blot, CCK-8 Assay, Flow Cytometry, Cell Counting, Negative Control, Reverse Transcription, Polymerase Chain Reaction

    TERF2 deficiency promotes apoptosis in AML cells. (A-D) Flow cytometry assay analyzed apoptosis in NC or TERF2-knockdown MOLM13 cells (A,B) or THP1 cells (C,D). (E-H) Western blot detected cleaved caspase 3 levels of NC or TERF2-knockdown MOLM13 cells (E,F) or THP1 cells (G,H). ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; NC, negative control.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: TERF2 deficiency promotes apoptosis in AML cells. (A-D) Flow cytometry assay analyzed apoptosis in NC or TERF2-knockdown MOLM13 cells (A,B) or THP1 cells (C,D). (E-H) Western blot detected cleaved caspase 3 levels of NC or TERF2-knockdown MOLM13 cells (E,F) or THP1 cells (G,H). ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; NC, negative control.

    Article Snippet: AML cell lines (MOLM13 and THP-1) were obtained from the American Type Culture Collection (ATCC) and were cultured in RPMI-1640 medium (Gibco, Grand Island, USA) containing 10% heat-inactivated fetal bovine serum (FBS; Gibco) under standard conditions (37 °C, 5% CO 2 ).

    Techniques: Flow Cytometry, Knockdown, Western Blot, Negative Control

    TERF2 involved in cuproptosis through E2F pathway in AML. (A) Bar graphs illustrate the associations between TERF2 expression levels and gene hallmark sets in AML patients. (B) GSEA for AML patients with high TERF2 expression in TCGA database. (C-E) Western blot analysis of E2F1, CDK4, CDK6, CDKN2A levels in MOLM13 cells and NB4 cells with or without TERF2 silence. (F,G) MOLM13 (F) and NB4 (G) cells with TERF2 knockdown were treated with specified concentrations of ES-Cu (1:1 ratio) for 48 hours, followed by cell viability assessment using the CCK-8 assay. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; ES-Cu, elesclomol-copper; GSEA, gene set enrichment analysis; IC 50 , half-maximal inhibitory concentration; TCGA, The Cancer Genome Atlas.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: TERF2 involved in cuproptosis through E2F pathway in AML. (A) Bar graphs illustrate the associations between TERF2 expression levels and gene hallmark sets in AML patients. (B) GSEA for AML patients with high TERF2 expression in TCGA database. (C-E) Western blot analysis of E2F1, CDK4, CDK6, CDKN2A levels in MOLM13 cells and NB4 cells with or without TERF2 silence. (F,G) MOLM13 (F) and NB4 (G) cells with TERF2 knockdown were treated with specified concentrations of ES-Cu (1:1 ratio) for 48 hours, followed by cell viability assessment using the CCK-8 assay. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; ES-Cu, elesclomol-copper; GSEA, gene set enrichment analysis; IC 50 , half-maximal inhibitory concentration; TCGA, The Cancer Genome Atlas.

    Article Snippet: AML cell lines (MOLM13 and THP-1) were obtained from the American Type Culture Collection (ATCC) and were cultured in RPMI-1640 medium (Gibco, Grand Island, USA) containing 10% heat-inactivated fetal bovine serum (FBS; Gibco) under standard conditions (37 °C, 5% CO 2 ).

    Techniques: Expressing, Western Blot, Knockdown, CCK-8 Assay, Cell Counting, Concentration Assay

    Knockdown of TERF2 suppresses AML progression and enhances cuproptosis sensitivity in vivo . (A,B) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted NSG mice (A) and the quantification of luciferase signals for all mice per group (B). (C) Kaplan-Meier analysis of survival of MOLM13-engrafted mice, log rank test. (D,E) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted mice treated with elesclomol (D) and the quantification of luciferase signals for all mice per group (E). (F) Kaplan-Meier analysis of survival of MOLM13-engrafted mice treated with elesclomol, log rank test. **, P<0.01. AML, acute myeloid leukemia; NSG, NOD-SCID IL2rg.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: Knockdown of TERF2 suppresses AML progression and enhances cuproptosis sensitivity in vivo . (A,B) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted NSG mice (A) and the quantification of luciferase signals for all mice per group (B). (C) Kaplan-Meier analysis of survival of MOLM13-engrafted mice, log rank test. (D,E) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted mice treated with elesclomol (D) and the quantification of luciferase signals for all mice per group (E). (F) Kaplan-Meier analysis of survival of MOLM13-engrafted mice treated with elesclomol, log rank test. **, P<0.01. AML, acute myeloid leukemia; NSG, NOD-SCID IL2rg.

    Article Snippet: AML cell lines (MOLM13 and THP-1) were obtained from the American Type Culture Collection (ATCC) and were cultured in RPMI-1640 medium (Gibco, Grand Island, USA) containing 10% heat-inactivated fetal bovine serum (FBS; Gibco) under standard conditions (37 °C, 5% CO 2 ).

    Techniques: Knockdown, In Vivo, Imaging, Luciferase

    A) Overall survival analysis of AML patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in AML cell lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, U937, and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) Overall survival analysis of AML patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in AML cell lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, U937, and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Expressing, MANN-WHITNEY, Mutagenesis, Activity Assay, Gene Expression, CRISPR, Control, Quantitative RT-PCR, Flow Cytometry, Phospho-proteomics, Western Blot

    A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations of CX-4945 and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations of CX-4945 and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Activity Assay, Staining, Flow Cytometry, Expressing

    A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Western Blot, Quantitative RT-PCR, Control

    A) Principal component analysis (PCA) plot showing the distribution of Molm-13 (parental) versus Molm-13/VR (with and without drug treatment for 24h) AML cell lines (n=2 out of three replicates). B) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in Molm-13 and Molm-13/VR AML cell lines transcriptome. C-D) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘B’ ( C ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( D ). E) Gene-Concept network analysis depicting the gene-to-gene interconnection in the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented with significant differentially expressed genes in Molm-13/VR cells with CX+VEN combo treatment (control vs. Combo). Node size refers to the number of genes in the enriched pathway. Genes shared between edges refer to terms belonging to multiple pathophysiological categories. F) Principal component analysis (PCA) plot showing the distribution of PDX 2016-7 (with and without drug treatment for 24h) AML cells (n=3). G) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in PDX 2016-7 AML cells transcriptome. H-I) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘G’ ( H ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( I ). J) Heatmap showing the expression profile of genes highly expressed in VEN non-responders (adapted from ), p53 target genes, and BCL2-family members (anti-apoptotic and pro-apoptotic) in PDX 2016-7 cells.

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) Principal component analysis (PCA) plot showing the distribution of Molm-13 (parental) versus Molm-13/VR (with and without drug treatment for 24h) AML cell lines (n=2 out of three replicates). B) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in Molm-13 and Molm-13/VR AML cell lines transcriptome. C-D) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘B’ ( C ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( D ). E) Gene-Concept network analysis depicting the gene-to-gene interconnection in the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented with significant differentially expressed genes in Molm-13/VR cells with CX+VEN combo treatment (control vs. Combo). Node size refers to the number of genes in the enriched pathway. Genes shared between edges refer to terms belonging to multiple pathophysiological categories. F) Principal component analysis (PCA) plot showing the distribution of PDX 2016-7 (with and without drug treatment for 24h) AML cells (n=3). G) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in PDX 2016-7 AML cells transcriptome. H-I) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘G’ ( H ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( I ). J) Heatmap showing the expression profile of genes highly expressed in VEN non-responders (adapted from ), p53 target genes, and BCL2-family members (anti-apoptotic and pro-apoptotic) in PDX 2016-7 cells.

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Functional Assay, Control, Expressing

    A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Derivative Assay, Irradiation, Injection, Transplantation Assay, Flow Cytometry, Western Blot

    A) Overall survival analysis of AML patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in AML cell lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, U937, and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) Overall survival analysis of AML patients with low and high expression of CSNK2A1 (probe ID: 212072_s_at) from TCGA data (AML vs normal; accessed from BloodSplot database at https://www.fobinf.com/ ). B) The plot depicts the median difference (95% confidence interval) of CK2α ( CSNK2A1 ) expression in the presence or absence of mutations in the indicated gene calculated using Mann-Whitney tests. The gene mutations that significantly (p<0.05) associated with increased CSNK2A1 expression were shown along with the sample number for mutated (denoted by M) and wildtype normal (denoted by N) in the BeatAML cohort. C) Volcano plot shows the association of gene mutation with venetoclax activity (accessed from BeatAML database at https://www.vizome.org/aml2/inhibitor/ ). Increased sensitivity is indicated by red, increased resistance indicated by blue as determined by the effect size (X-axis). D) Correlation between CSNK2A1 (CK2α) and BCL2L1 (BCL-XL) gene expression levels from Beat AML patient samples as determined by both Spearman and Pearson correlation coefficients. E) Heatmap summarizing the average log 2 fold change of sgRNA abundance in kinase domain-focused CRISPR screening in AML cell lines (data adapted from ). F) Enrichment of individual sgRNAs for genes encoding CK2 catalytic subunit ( CSNK2A1 ) and regulatory subunit ( CSNK2B ), BCL-XL ( BCL2L1 ), MCL1, and TP53 plotted as log-fold change over control cells following 14 days of treatment with 0.5-1µM VEN in a CRISPR drop-out screening (data adopted from [ , ]). Genes encoding BCL-XL, MCL1, and TP53 were used as known controls that alter VEN activity. Data are presented as Mean ± SEM (n=4-5 sgRNAs targeting each gene). G ) Parental and VR-AML cell lines were treated with different concentrations of venetoclax for 48 h and assessed for cell viability using WST. H) The basal level expression of indicated genes was assessed in different AML cell lines by qRT-PCR. The data are presented as mean ± SEM (n=3 replicates from a representative run). *p<0.05 and **p<0.01 by unpaired t-test (Welch’s correction) denotes statistical significance. I ) Schematic presentation of AML cells profiling with BH3 peptides (activators: BIM, BID; and sensitizer: PUMA) for the assessment of cytochrome c (Cyt C) release. Created with BioRender.com . J) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides and calculated the delta priming. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. K) The surface expression of chemoresistance markers (CD47 and CD123) on Molm-13, Molm-13VR, U937, and PDX 2016-7 cells was analyzed using flow cytometry. L ) The basal level expression of CK2α, CK2 substrate phosphorylation, and other BCL2 family members in parental and VR-AML cell lines was analyzed by western blotting.

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Expressing, MANN-WHITNEY, Mutagenesis, Activity Assay, Gene Expression, CRISPR, Control, Quantitative RT-PCR, Flow Cytometry, Phospho-proteomics, Western Blot

    A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations of CX-4945 and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) AML cell lines including both VEN-susceptible and resistant (Molm-13, Molm-13/VR, HL-60, HL-60/VR, U937), and AML PDX cells (2016-1, 2016-7) were treated with different concentrations of CX-4945 and VEN alone or in combination with indicated doses for 48 h. Cell viability was assessed using WST reagent and cell viability was calculated relative to vehicle-treated cells as 100%. B) ZIP synergy scores for CX-4945 and VEN combination in different AML cell lines and PDX cells were shown. ZIP scores greater than 10 indicates ‘synergy’, and 0-10 indicate ‘additive’ activity between CX-4945 and VEN. C-D) AML cells (Molm-13, Molm-13/VR, PDX 2016-7) were treated with CX-4945 and VEN alone or in combination for 24 h and stained with Annexin V/7AAD for analyzing apoptosis by flow cytometry ( C ). Relative apoptosis was calculated by normalizing to vehicle treated cells ( D ). The data are presented as mean ± SD (n=2-4). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 by one-way ANOVA (Holm-Sidak’s multiple comparisons test) denotes statistical significance. E) AML cell lines (Molm-13, Molm-13/VR) were treated with CX-4945 and VEN alone or in combination for 24 h and the surface expression of chemoresistance markers (CD47 and CD123) was analyzed by flow cytometry. F) Schematic showing the workflow for dynamic BH3 profiling to measure drug-induced priming of BH3 peptides in AML cells. The difference in Cyt c release (%) with and without drug treatment was presented as delta priming. Created with BioRender.com . G) Molm-13 and Molm-13/VR cells were tested for Cyt C release by priming with BH3 peptides with and without CX-4945 treatment and calculated the delta priming. The data are presented as mean ± SEM (n=2) and analyzed by two-way ANOVA (Sidak’s multiple comparisons test).

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Activity Assay, Staining, Flow Cytometry, Expressing

    A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) The common mechanisms that govern cellular MCL-1 levels at transcription, translation, and post-translation levels are depicted. The signaling cascade mediated through CK2, PI3K/AKT, and mTOR regulate transcription and translation of MCL-1 isoforms (L-large, S-short, ES-extra short). MCL-1L (anti-apoptotic) undergoes caspase-mediated cleavage to form pro-apoptotic shorter MCL-1 isoforms (S & ES) that can induce cellular apoptosis independent of BAX and BAK. Created using BioRender.com . B) The levels of MCL-1 isoforms (L and ES) were measured by immunoblotting in AML cell lines and PDX cells after 24h of treatment with CX-4945 and VEN alone or in combination. C) Quantification of MCL-1 transcript levels after treatment with CX-4945 and VEN alone or in combination for 24h in indicated AML cell lines and PDX cells by qRT-PCR. The data are presented as mean ± SD (n=3) and analyzed by two-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 are considered statistically significant. D) Immunoblotting analysis of AML cell lines (Molm-13, Molm-13/VR, U937) and PDX (2016-1, 2016-7) cells after 24h of treatment with CX-4945 and VEN alone or in combination. β-Actin was used as a loading control. Representative blots from two to three independent experiments were shown.

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Western Blot, Quantitative RT-PCR, Control

    A) Principal component analysis (PCA) plot showing the distribution of Molm-13 (parental) versus Molm-13/VR (with and without drug treatment for 24h) AML cell lines (n=2 out of three replicates). B) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in Molm-13 and Molm-13/VR AML cell lines transcriptome. C-D) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘B’ ( C ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( D ). E) Gene-Concept network analysis depicting the gene-to-gene interconnection in the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented with significant differentially expressed genes in Molm-13/VR cells with CX+VEN combo treatment (control vs. Combo). Node size refers to the number of genes in the enriched pathway. Genes shared between edges refer to terms belonging to multiple pathophysiological categories. F) Principal component analysis (PCA) plot showing the distribution of PDX 2016-7 (with and without drug treatment for 24h) AML cells (n=3). G) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in PDX 2016-7 AML cells transcriptome. H-I) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘G’ ( H ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( I ). J) Heatmap showing the expression profile of genes highly expressed in VEN non-responders (adapted from ), p53 target genes, and BCL2-family members (anti-apoptotic and pro-apoptotic) in PDX 2016-7 cells.

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) Principal component analysis (PCA) plot showing the distribution of Molm-13 (parental) versus Molm-13/VR (with and without drug treatment for 24h) AML cell lines (n=2 out of three replicates). B) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in Molm-13 and Molm-13/VR AML cell lines transcriptome. C-D) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘B’ ( C ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( D ). E) Gene-Concept network analysis depicting the gene-to-gene interconnection in the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented with significant differentially expressed genes in Molm-13/VR cells with CX+VEN combo treatment (control vs. Combo). Node size refers to the number of genes in the enriched pathway. Genes shared between edges refer to terms belonging to multiple pathophysiological categories. F) Principal component analysis (PCA) plot showing the distribution of PDX 2016-7 (with and without drug treatment for 24h) AML cells (n=3). G) Heatmap showing the hierarchical clustering (k-means) of most variable genes (n=2000) in PDX 2016-7 AML cells transcriptome. H-I) Dot plot displaying the top-ranked functional pathways (MSigDB hallmark gene set) overrepresented in different gene clusters obtained with k-means clustering as shown in ‘G’ ( H ) or the differentially expressed genes with fold change >1.5 and adj-p <0.05 ( I ). J) Heatmap showing the expression profile of genes highly expressed in VEN non-responders (adapted from ), p53 target genes, and BCL2-family members (anti-apoptotic and pro-apoptotic) in PDX 2016-7 cells.

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Functional Assay, Control, Expressing

    A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.

    Journal: bioRxiv

    Article Title: CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteins

    doi: 10.64898/2025.12.24.696284

    Figure Lengend Snippet: A) Schematic depicting the treatment plan in AML patient-derived xenograft (PDX) mouse model. Similar scheme followed for cell line-derived xenograft (CDX) mice except the analysis after two-weeks of treatment. The NRG-S mice were irradiated and intravenously injected with AML cell lines Molm-13VR (0.25×10 6 cells/mouse), U937 (1×10 4 cells/mouse), and PDX 2016-7 (0.5×10 6 cells/mouse) and randomized into experimental groups (Vehicle, CX-4945, VEN, and CX+VEN Como). The drug treatment started after one week of cell transplantation and followed up for survival analysis or analysis after two-weeks of treatment (only for PDX). B-F) After two weeks of drug treatment, mice injected with PDX 2016-7 cells were sacrificed and spleen weight was recorded ( B ). The cells collected from spleens were analyzed by flow cytometry to analyze percent hCD45 positive cells ( C ). D-F) CBC analysis was performed on PDX 2016-7 mice after two-weeks of drug treatment by Hemavet analyzer. The data for B-F are presented as mean ± SD (n=7-8) and analyzed by one-way ANOVA (Tukey’s multiple comparisons test). *p<0.05, **p<0.01, ***p<0.001, and ****p<0.0001 indicates statistical significance, while ‘ns’ denotes ‘not significant’. G) Immunoblotting analysis of spleen cells collected from PDX 2016-7 mice after two-weeks of treatment with CX-4945, VEN, and CX+VEN combo. The data for three different experimental animals was presented. H-J) Kaplan-Meyer survival analysis of 2016-7 PDX ( H ), Molm-13/VR CDX ( I ), and U937 CDX ( J ) mice after treatment with CX-4945, VEN and CX+VEN combo. The overall median survival (MS) days for each experimental group of PDX and CDX mice were provided next to the legend. *p<0.05, **p<0.01 and ***p<0.001 by Gehan-Breslow-Wilcoxon test indicates statistical significance.

    Article Snippet: The human AML cell lines U937 (#CRL-1593.2), HL-60 (#CCL-240), THP-1 (#TIB-202), K562 (#CCL-243) were obtained from the American Type Culture Collection (ATCC) and MOLM-13 (#ACC554) cells were purchased from the German Collection of Microorganisms and Cell Cultures (DSMZ).

    Techniques: Derivative Assay, Irradiation, Injection, Transplantation Assay, Flow Cytometry, Western Blot