human t all cell lines jurkat  (ATCC)


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    Structured Review

    ATCC human t all cell lines jurkat
    The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in <t>T-ALL</t> Cells (A) Human T-ALL cell lines <t>Jurkat</t> (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p
    Human T All Cell Lines Jurkat, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions"

    Article Title: A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2018.09.025

    The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p
    Figure Legend Snippet: The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p

    Techniques Used: Infection, Immunostaining

    2) Product Images from "Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response"

    Article Title: Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response

    Journal: Oncotarget

    doi: 10.18632/oncotarget.12246

    Glutathione synthesis is partially involved in adipocyte protection of ALL cells ( A ) Intracellular GSH quantification in 3T3-L1 adipocytes ( n = 3). Viable cell number of BV173 and Nalm6 cells treated with DNR (100 and 200 nM, respectively) while co-cultured with 3T3-L1 ( B ) or ChubS7 ( C ) adipocytes that were pre-treated with 20 mM BSO for 24 hours ( n = 8–10). ( D ) Viable cell number of BV173 and Nalm6 cells treated with DNR while co-cultured with 3T3-L1 adipocytes that were pre-treated with 250 nM AUR for 24 hours ( n = 3).* p
    Figure Legend Snippet: Glutathione synthesis is partially involved in adipocyte protection of ALL cells ( A ) Intracellular GSH quantification in 3T3-L1 adipocytes ( n = 3). Viable cell number of BV173 and Nalm6 cells treated with DNR (100 and 200 nM, respectively) while co-cultured with 3T3-L1 ( B ) or ChubS7 ( C ) adipocytes that were pre-treated with 20 mM BSO for 24 hours ( n = 8–10). ( D ) Viable cell number of BV173 and Nalm6 cells treated with DNR while co-cultured with 3T3-L1 adipocytes that were pre-treated with 250 nM AUR for 24 hours ( n = 3).* p

    Techniques Used: Cell Culture

    Adipocytes protect ALL cells from oxidative stress ( A ) Measurement of % ROS high population in Nalm6 cells treated with DNR for 6 hours. % ROS high based on gates defined by cells without DNR treatment. Adipo condition is significantly different than both Fibro and No Feeder by repeated measure ANOVA ( p
    Figure Legend Snippet: Adipocytes protect ALL cells from oxidative stress ( A ) Measurement of % ROS high population in Nalm6 cells treated with DNR for 6 hours. % ROS high based on gates defined by cells without DNR treatment. Adipo condition is significantly different than both Fibro and No Feeder by repeated measure ANOVA ( p

    Techniques Used:

    ALL cells induce oxidative stress in adipocytes ( A ) Representative fluorescent confocal microscopy images of 3T3-L1 adipocytes alone, with ALL in TransWells, or treated with 20 mM BSO for 48 hours. Top: DCF (green) only, bottom: DIC images. ( B ) Quantification of fluorescence (FITC) from 3 images similar to A. *indicate t -tests on log-transformed pixel counts. ( C ) 3T3-L1 gene expression by qPCR with (gray bar) and without (white bar) 8093 cells; n = 3. ( D ) Western blot of HO-1 expression in 3T3-L1 adipocytes exposed to DNR, ALL, or both. GAPDH was used as loading control. E. GSH levels measured in media after conditioning with BV173 ALL cells, 3T3-L1 adipocytes, or both, for 48 hours. * P
    Figure Legend Snippet: ALL cells induce oxidative stress in adipocytes ( A ) Representative fluorescent confocal microscopy images of 3T3-L1 adipocytes alone, with ALL in TransWells, or treated with 20 mM BSO for 48 hours. Top: DCF (green) only, bottom: DIC images. ( B ) Quantification of fluorescence (FITC) from 3 images similar to A. *indicate t -tests on log-transformed pixel counts. ( C ) 3T3-L1 gene expression by qPCR with (gray bar) and without (white bar) 8093 cells; n = 3. ( D ) Western blot of HO-1 expression in 3T3-L1 adipocytes exposed to DNR, ALL, or both. GAPDH was used as loading control. E. GSH levels measured in media after conditioning with BV173 ALL cells, 3T3-L1 adipocytes, or both, for 48 hours. * P

    Techniques Used: Confocal Microscopy, Fluorescence, Transformation Assay, Expressing, Real-time Polymerase Chain Reaction, Western Blot

    Oxidative stress in adipocytes leads to secretion of survival factors that protect ALL cells from DNR ( A ) Representative western blot of HIF-1α in ChubS7 adipocytes treated with CoCl 2 . GAPDH was used as loading control. ( B ) 3T3-L1 gene expression by qPCR with CoCl 2 treatment for 24 hours ( n = 4). ( C ) Viable cell number of DNR-treated 8093 ALL cells (left) or BV173 cells (right) in the presence of ACM from 3T3-L1 or ChubS7. ACM spiked with CoCl 2 were denoted as (+ CoCl 2 ) and ACM conditioned in the presence of 30 μM CoCl 2 as (w/ CoCl 2 , n = 4–8). * P
    Figure Legend Snippet: Oxidative stress in adipocytes leads to secretion of survival factors that protect ALL cells from DNR ( A ) Representative western blot of HIF-1α in ChubS7 adipocytes treated with CoCl 2 . GAPDH was used as loading control. ( B ) 3T3-L1 gene expression by qPCR with CoCl 2 treatment for 24 hours ( n = 4). ( C ) Viable cell number of DNR-treated 8093 ALL cells (left) or BV173 cells (right) in the presence of ACM from 3T3-L1 or ChubS7. ACM spiked with CoCl 2 were denoted as (+ CoCl 2 ) and ACM conditioned in the presence of 30 μM CoCl 2 as (w/ CoCl 2 , n = 4–8). * P

    Techniques Used: Western Blot, Expressing, Real-time Polymerase Chain Reaction

    Exogenous antioxidants protect ALL cells from DNR ( A ) BV173 and Nalm6 treated with DNR or DNR + GSH (20 mM, n = 4). ( B ) BV173 and Nalm6 treated with DNR or DNR + NAC (20 mM, n = 3–4). ( C ) Cell viability and intracellular ROS evaluation using flow cytometry with DAPI and CellROX ® staining of BV173 (top two panels) and Nalm6 (bottom two panels) treated with DNR alone or DNR and NAC n = 5. * P
    Figure Legend Snippet: Exogenous antioxidants protect ALL cells from DNR ( A ) BV173 and Nalm6 treated with DNR or DNR + GSH (20 mM, n = 4). ( B ) BV173 and Nalm6 treated with DNR or DNR + NAC (20 mM, n = 3–4). ( C ) Cell viability and intracellular ROS evaluation using flow cytometry with DAPI and CellROX ® staining of BV173 (top two panels) and Nalm6 (bottom two panels) treated with DNR alone or DNR and NAC n = 5. * P

    Techniques Used: Flow Cytometry, Cytometry, Staining

    Adipocytes protect ALL from oxidative stress induced cell death ( A ) ALL cells co-cultured in TransWells over 3T3-L1 and ChubS7 pre-adipocytes (hatched bars) and adipocytes (black bars) with 72 hour DNR treatment (8093 35 nM, BV173 100 nM, RS4;11 100 nM, and Nalm6 200 nM). No feeder condition is where ALL cells were cultured alone ( n = 3–5). ( B ) One representative image of western blot of Caspase 3 (37 kDa) and cleaved caspase 3 (19 and 17 kDa) in BV173 cells treated with DNR for 24 hours in the presence or absence of adipocytes. Images were histogram stretched in a consistent manner to increase brightness for publication. Quantification of the ratio of cleaved (both bands) over total caspase 3 (band at 37 kDa) is shown on the right ( n = 3). ( C ) BV173 ALL cells cultured over 3T3-L1 cells and treated with various doses of doxorubicin (Dox). ( D ) 8093 cells treated with 35 nM DNR in 3T3-L1 ACM and ALCM (left, n = 6); BV173 cells treated with 100 nM DNR in ChubS7 ACM and ALCM (right, n = 5). ( E ) Quantification of cleaved over total caspase 3 of 8093 ALL cells after 24 hours treatment with 25 nM DNR with and without ALCM. ( F ) Annexin V staining of human ALL cells after 24 hour exposure to DNR with or without ALCM. * P
    Figure Legend Snippet: Adipocytes protect ALL from oxidative stress induced cell death ( A ) ALL cells co-cultured in TransWells over 3T3-L1 and ChubS7 pre-adipocytes (hatched bars) and adipocytes (black bars) with 72 hour DNR treatment (8093 35 nM, BV173 100 nM, RS4;11 100 nM, and Nalm6 200 nM). No feeder condition is where ALL cells were cultured alone ( n = 3–5). ( B ) One representative image of western blot of Caspase 3 (37 kDa) and cleaved caspase 3 (19 and 17 kDa) in BV173 cells treated with DNR for 24 hours in the presence or absence of adipocytes. Images were histogram stretched in a consistent manner to increase brightness for publication. Quantification of the ratio of cleaved (both bands) over total caspase 3 (band at 37 kDa) is shown on the right ( n = 3). ( C ) BV173 ALL cells cultured over 3T3-L1 cells and treated with various doses of doxorubicin (Dox). ( D ) 8093 cells treated with 35 nM DNR in 3T3-L1 ACM and ALCM (left, n = 6); BV173 cells treated with 100 nM DNR in ChubS7 ACM and ALCM (right, n = 5). ( E ) Quantification of cleaved over total caspase 3 of 8093 ALL cells after 24 hours treatment with 25 nM DNR with and without ALCM. ( F ) Annexin V staining of human ALL cells after 24 hour exposure to DNR with or without ALCM. * P

    Techniques Used: Cell Culture, Western Blot, Staining

    3) Product Images from "Regulatory Phosphorylation of Ikaros by Bruton's Tyrosine Kinase"

    Article Title: Regulatory Phosphorylation of Ikaros by Bruton's Tyrosine Kinase

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0071302

    Co-localization and Physical Interactions of Native Ikaros and BTK Proteins in Human Cells. [A] Nuclear co-localization of Native IK and BTK. ALL-N1 cells were fixed and stained with polyclonal rabbit anti-IK1 (primary Ab)/Alexa Fluor 568 F(ab') 2 fragment of goat anti-rabbit IgG (secondary Ab) (red) and mouse anti-BTK MoAb (primary Ab)/Alexa Fluor 488 goat anti-mouse IgG (secondary Ab) (green) antibodies. Nuclei were stained with blue fluorescent dye 4′,6-diamidino-2-phenylindole (DAPI). MERGE panels depict the merge three-color confocal image showing co-localization of IK1 and BTK in DAPI-stained nucleus as magenta immunofluorescent foci (System magnification: 315×). Representative foci of colocalization are indicated with white arrowheads. [B] Co-immunoprecipitation of Native IK and BTK. B1 depicts the results of the BTK Western blot analysis of the IK and BTK immune complexes immunoprecipitated (IP) from ALL-N1 cells. B.2 depicts the results of the IK Western blot analysis of the BTK and IK immune complexes from the same cells. Controls included immunoprecipitations performed without using a primary (1 0 ) antibody.
    Figure Legend Snippet: Co-localization and Physical Interactions of Native Ikaros and BTK Proteins in Human Cells. [A] Nuclear co-localization of Native IK and BTK. ALL-N1 cells were fixed and stained with polyclonal rabbit anti-IK1 (primary Ab)/Alexa Fluor 568 F(ab') 2 fragment of goat anti-rabbit IgG (secondary Ab) (red) and mouse anti-BTK MoAb (primary Ab)/Alexa Fluor 488 goat anti-mouse IgG (secondary Ab) (green) antibodies. Nuclei were stained with blue fluorescent dye 4′,6-diamidino-2-phenylindole (DAPI). MERGE panels depict the merge three-color confocal image showing co-localization of IK1 and BTK in DAPI-stained nucleus as magenta immunofluorescent foci (System magnification: 315×). Representative foci of colocalization are indicated with white arrowheads. [B] Co-immunoprecipitation of Native IK and BTK. B1 depicts the results of the BTK Western blot analysis of the IK and BTK immune complexes immunoprecipitated (IP) from ALL-N1 cells. B.2 depicts the results of the IK Western blot analysis of the BTK and IK immune complexes from the same cells. Controls included immunoprecipitations performed without using a primary (1 0 ) antibody.

    Techniques Used: Staining, Immunoprecipitation, Western Blot

    4) Product Images from "Targeting of heme oxygenase-1 attenuates the negative impact of Ikaros isoform 6 in adult BCR-ABL1-positive B-ALL"

    Article Title: Targeting of heme oxygenase-1 attenuates the negative impact of Ikaros isoform 6 in adult BCR-ABL1-positive B-ALL

    Journal: Oncotarget

    doi: 10.18632/oncotarget.10725

    The expression of HO-1 is strongly correlated with IK6 A. Differential expression of HO-1 mRNA in adult BCR-ABL1-positive B-ALL patients and normal CD34 + cells were determined by qRT-PCR. B. Western blot analysis of Ikaros expression in IK6-positive and –negative patients. C, D. Western blot analysis of HO-1 expression at protein level in adult BCR-ABL1-positive B-ALL patients and normal CD34 + cells. E. Scatterplot representation of the correlation between the expression of HO-1 and Ikaros in patient samples. F. Co-immunoprecipitation assay to verify the interaction of Flag-IK6 with Myc-HO-1 in SupB15 cells (upper panel) and the endogenous interaction of Ikaros with HO-1 in primary leukemic cells (lower panel). (Pts=patients).
    Figure Legend Snippet: The expression of HO-1 is strongly correlated with IK6 A. Differential expression of HO-1 mRNA in adult BCR-ABL1-positive B-ALL patients and normal CD34 + cells were determined by qRT-PCR. B. Western blot analysis of Ikaros expression in IK6-positive and –negative patients. C, D. Western blot analysis of HO-1 expression at protein level in adult BCR-ABL1-positive B-ALL patients and normal CD34 + cells. E. Scatterplot representation of the correlation between the expression of HO-1 and Ikaros in patient samples. F. Co-immunoprecipitation assay to verify the interaction of Flag-IK6 with Myc-HO-1 in SupB15 cells (upper panel) and the endogenous interaction of Ikaros with HO-1 in primary leukemic cells (lower panel). (Pts=patients).

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Co-Immunoprecipitation Assay

    IK6 is highly expressed in adult BCR-ABL1-positive B-ALL patients A. Schematic diagram of the full-length IKZF1 cDNA and the different isoforms detected in our samples. F: N-terminal zinc-fingers show DNA-binding activity, and C-terminal zinc fingers mediate dimerization of the protein. Ex indicates exon. B. Expressions of the different IKZF1 isoforms in 42 BCR-ABL1-positive B-ALLsamples were determined by RT-PCR. IK1(945bp), IK2(884bp), IK4 (458bp), IK6(255bp). C. Sequencing analysis of IK6 isoform in which exon 3 is juxtaposed with exon8. D. Kaplan-meier estimation of DFS in IK6-positive and -negative group. E. Cumulative incidence of relapse curves by IKZF1 status in our samples, with 3-year estimates. CR1, first complete remission.
    Figure Legend Snippet: IK6 is highly expressed in adult BCR-ABL1-positive B-ALL patients A. Schematic diagram of the full-length IKZF1 cDNA and the different isoforms detected in our samples. F: N-terminal zinc-fingers show DNA-binding activity, and C-terminal zinc fingers mediate dimerization of the protein. Ex indicates exon. B. Expressions of the different IKZF1 isoforms in 42 BCR-ABL1-positive B-ALLsamples were determined by RT-PCR. IK1(945bp), IK2(884bp), IK4 (458bp), IK6(255bp). C. Sequencing analysis of IK6 isoform in which exon 3 is juxtaposed with exon8. D. Kaplan-meier estimation of DFS in IK6-positive and -negative group. E. Cumulative incidence of relapse curves by IKZF1 status in our samples, with 3-year estimates. CR1, first complete remission.

    Techniques Used: Zinc-Fingers, Binding Assay, Activity Assay, Reverse Transcription Polymerase Chain Reaction, Sequencing

    5) Product Images from "UTX inhibition as selective epigenetic therapy against TAL1-driven T-cell acute lymphoblastic leukemia"

    Article Title: UTX inhibition as selective epigenetic therapy against TAL1-driven T-cell acute lymphoblastic leukemia

    Journal: Genes & Development

    doi: 10.1101/gad.276790.115

    The H3K27 demethylase inhibitor GSK-J4 is efficient in vivo against patient-derived xenotransplant models of TAL1-positive T-ALL. ( A ) Experimental strategy. NSG mice were transplanted by intrafemoral (IF) injection of primary human T-ALL cells. When the
    Figure Legend Snippet: The H3K27 demethylase inhibitor GSK-J4 is efficient in vivo against patient-derived xenotransplant models of TAL1-positive T-ALL. ( A ) Experimental strategy. NSG mice were transplanted by intrafemoral (IF) injection of primary human T-ALL cells. When the

    Techniques Used: In Vivo, Derivative Assay, Mouse Assay, Injection

    6) Product Images from "Matrine induced G0/G1 arrest and apoptosis in human acute T-cell lymphoblastic leukemia (T-ALL) cells"

    Article Title: Matrine induced G0/G1 arrest and apoptosis in human acute T-cell lymphoblastic leukemia (T-ALL) cells

    Journal: Bosnian Journal of Basic Medical Sciences

    doi: 10.17305/bjbms.2017.2457

    Hierarchical clustering of the RNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 49 RNAs, 24 were upregulated and 3 were downregulated and exhibited ≥2-fold change in expression relative to the untreated CCRF-CEM control cells. All experiments were performed in triplicate and Hs18s, GAPDH , and HPRT1 were used as housekeeping controls. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. CDKN1A ( p = 0.000159), IL6 ( p = 0.000011), KDR ( p = 0.001288), and VEGFC ( p = 0.000004) gene expressions were prominently upregulated, whereas BCL 2 ( p = 0.002893), CDKN 3 ( p = 0.000024), and E2F 1 ( p = 0.000128) gene expressions were downregulated in matrine-treated CCRF-CEM cells compared with untreated control CCRF-CEM cells.
    Figure Legend Snippet: Hierarchical clustering of the RNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 49 RNAs, 24 were upregulated and 3 were downregulated and exhibited ≥2-fold change in expression relative to the untreated CCRF-CEM control cells. All experiments were performed in triplicate and Hs18s, GAPDH , and HPRT1 were used as housekeeping controls. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. CDKN1A ( p = 0.000159), IL6 ( p = 0.000011), KDR ( p = 0.001288), and VEGFC ( p = 0.000004) gene expressions were prominently upregulated, whereas BCL 2 ( p = 0.002893), CDKN 3 ( p = 0.000024), and E2F 1 ( p = 0.000128) gene expressions were downregulated in matrine-treated CCRF-CEM cells compared with untreated control CCRF-CEM cells.

    Techniques Used: RNA Expression, Expressing

    Hierarchical clustering of the miRNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 44 miRNAs, 42 were downregulated and exhibited ≥2-fold change in expression relative to untreated control CCRF-CEM cells. All experiments were performed in triplicate and RNU6-2 was used as an endogenous control. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. Hsa-miR-376b-3p ( p = 0.008), hsa-miR-106b-3p ( p = 0.028), hsa-miR-20a-3p ( p = 0.014), hsa-miR-519a-3p ( p = 0.00534), and hsa-miR-204-5p ( p = 0.001) expression levels were significantly decreased in the matrine-treated compared to untreated control cells.
    Figure Legend Snippet: Hierarchical clustering of the miRNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 44 miRNAs, 42 were downregulated and exhibited ≥2-fold change in expression relative to untreated control CCRF-CEM cells. All experiments were performed in triplicate and RNU6-2 was used as an endogenous control. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. Hsa-miR-376b-3p ( p = 0.008), hsa-miR-106b-3p ( p = 0.028), hsa-miR-20a-3p ( p = 0.014), hsa-miR-519a-3p ( p = 0.00534), and hsa-miR-204-5p ( p = 0.001) expression levels were significantly decreased in the matrine-treated compared to untreated control cells.

    Techniques Used: Expressing

    7) Product Images from "MicroRNA-223 decreases cell proliferation, migration, invasion, and enhances cell apoptosis in childhood acute lymphoblastic leukemia via targeting Forkhead box O 1"

    Article Title: MicroRNA-223 decreases cell proliferation, migration, invasion, and enhances cell apoptosis in childhood acute lymphoblastic leukemia via targeting Forkhead box O 1

    Journal: Bioscience Reports

    doi: 10.1042/BSR20200485

    miR-223 inhibited the cell proliferation, colony formation ability and promoted cell apoptosis in ALL ( A ) The mRNA expression of miR-223 in CCRF-CEM and NALM-6 cells was detected by qRT-PCR. ( B ) The OD 450 value of CCRF-CEM and NALM-6 cells was determined by MTT assay. ( C ) The number of CCRF-CEM and NALM-6 cell colonies was confirmed by colony formation assay. ( D ) The apoptosis of CCRF-CEM and NALM-6 cells was detected by flow cytometry. **P
    Figure Legend Snippet: miR-223 inhibited the cell proliferation, colony formation ability and promoted cell apoptosis in ALL ( A ) The mRNA expression of miR-223 in CCRF-CEM and NALM-6 cells was detected by qRT-PCR. ( B ) The OD 450 value of CCRF-CEM and NALM-6 cells was determined by MTT assay. ( C ) The number of CCRF-CEM and NALM-6 cell colonies was confirmed by colony formation assay. ( D ) The apoptosis of CCRF-CEM and NALM-6 cells was detected by flow cytometry. **P

    Techniques Used: Expressing, Quantitative RT-PCR, MTT Assay, Colony Assay, Flow Cytometry

    FOXO1 reversed the effects of miR-223 in ALL cells ( A ) The protein expression of FOXO1in NALM-6 cells was detected by Western blot; ** P
    Figure Legend Snippet: FOXO1 reversed the effects of miR-223 in ALL cells ( A ) The protein expression of FOXO1in NALM-6 cells was detected by Western blot; ** P

    Techniques Used: Expressing, Western Blot

    miR-223 inhibited the cell invasion and migration in ALL ( A and B ) The number of invasion and migration cells in CCRF-CEM and NALM-6 cells was measured by transwell assay; magnification, ×200) **P
    Figure Legend Snippet: miR-223 inhibited the cell invasion and migration in ALL ( A and B ) The number of invasion and migration cells in CCRF-CEM and NALM-6 cells was measured by transwell assay; magnification, ×200) **P

    Techniques Used: Migration, Transwell Assay

    8) Product Images from "A Cell-Targeted, Size-Photocontrollable, Nuclear-Uptake Nanodrug Delivery System for Drug-Resistant Cancer Therapy"

    Article Title: A Cell-Targeted, Size-Photocontrollable, Nuclear-Uptake Nanodrug Delivery System for Drug-Resistant Cancer Therapy

    Journal: Nano Letters

    doi: 10.1021/nl503777s

    Specific cell binding and photocontrolled intracellular distribution of NP/NR-Sgc8s.(A) Flow cytometry assay proving the specific binding of Sgc8, NR-Sgc8, and NP/NR-Sgc8 to target CEM cells not to nontarget Ramos cells (Lib represents a random library sequence). (B) CLSM images of CEM cells after treatment with 15-NP/NR-Sgc8s without (i) and with (ii) NIR irradiation or after treatment with 8.5-NP/NR-Sgc8s without (iii) and with (iv) NIR irradiation. From left to right: fluorescence image for NP-TMR, NR-Cy5, and overlay of the NP-TMR, NR-Cy5, and Hoechst 33342 fluorescence channels plus the bright field channel. The scale bar represents 5 μm.
    Figure Legend Snippet: Specific cell binding and photocontrolled intracellular distribution of NP/NR-Sgc8s.(A) Flow cytometry assay proving the specific binding of Sgc8, NR-Sgc8, and NP/NR-Sgc8 to target CEM cells not to nontarget Ramos cells (Lib represents a random library sequence). (B) CLSM images of CEM cells after treatment with 15-NP/NR-Sgc8s without (i) and with (ii) NIR irradiation or after treatment with 8.5-NP/NR-Sgc8s without (iii) and with (iv) NIR irradiation. From left to right: fluorescence image for NP-TMR, NR-Cy5, and overlay of the NP-TMR, NR-Cy5, and Hoechst 33342 fluorescence channels plus the bright field channel. The scale bar represents 5 μm.

    Techniques Used: Binding Assay, Flow Cytometry, Cytometry, Sequencing, Confocal Laser Scanning Microscopy, Irradiation, Fluorescence

    Cytotoxicity assay. Viability of CEM cells (A) and Ramos cells (B) with different treatments. The error bars represent the standard deviation of three independent experiments.
    Figure Legend Snippet: Cytotoxicity assay. Viability of CEM cells (A) and Ramos cells (B) with different treatments. The error bars represent the standard deviation of three independent experiments.

    Techniques Used: Cytotoxicity Assay, Standard Deviation

    9) Product Images from "Detection of E2A-PBX1 fusion transcripts in human non-small-cell lung cancer"

    Article Title: Detection of E2A-PBX1 fusion transcripts in human non-small-cell lung cancer

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    doi: 10.1186/1756-9966-32-29

    Detection of E2A-PBX1 fusion transcripts in NSCLC. Semi-quantitative RT-PCR in NSCLC tissues ( A ) and cell lines ( B ). GAPDH was used as internal control. RCH-ACV and CCRF-CEM were regarded as positive (marked by +) and negative (marked by -) controls, respectively. 23 positive specimens (#1-23), 6 selected negative samples (#24-29) and adult normal lung tissue (#30) were shown in ( A ). ( C ) Sequencing results of RCH-ACV, H1666 and tissue #1. Partial region around the junction site (indicated by an arrow and a dashed line) was shown. The numbers showed the positions of the sequence according to E2A (NM_003200) and PBX1 (NM_002585) mRNA sequences.
    Figure Legend Snippet: Detection of E2A-PBX1 fusion transcripts in NSCLC. Semi-quantitative RT-PCR in NSCLC tissues ( A ) and cell lines ( B ). GAPDH was used as internal control. RCH-ACV and CCRF-CEM were regarded as positive (marked by +) and negative (marked by -) controls, respectively. 23 positive specimens (#1-23), 6 selected negative samples (#24-29) and adult normal lung tissue (#30) were shown in ( A ). ( C ) Sequencing results of RCH-ACV, H1666 and tissue #1. Partial region around the junction site (indicated by an arrow and a dashed line) was shown. The numbers showed the positions of the sequence according to E2A (NM_003200) and PBX1 (NM_002585) mRNA sequences.

    Techniques Used: Quantitative RT-PCR, Sequencing

    10) Product Images from "ARRB1-promoted NOTCH1 degradation is suppressed by oncomiR miR-223 in T cell acute lymphoblastic leukemia"

    Article Title: ARRB1-promoted NOTCH1 degradation is suppressed by oncomiR miR-223 in T cell acute lymphoblastic leukemia

    Journal: Cancer research

    doi: 10.1158/0008-5472.CAN-19-1471

    ARRB1 inhibits the tumor progression of human T-ALL cells. (A) GFP- and firefly luciferase-tagged Jurkat cells with ARRB1 overexpression (β1) or knockdown (sh-1 and sh-2) were tail-vein injected into irradiated NOD/SCID mice (n=5 per group). Twenty-one days after injection, bioluminescence images were obtained after administrating the mice D-Luciferin sodium salt. Subsequently, the mice were sacrificed, the spleens were spliced and stained with an anti-CD45RA antibody, and the bone marrow of the femurs was flushed out and subjected to anti-GFP immunostaining to assess the leukemia burden. Black scale bar, 500 μm; white scale bar, 100 μm. (B) The histogram shows the scores for the CD45RA + cells in the spleens. Image Pro Plus was used to calculate the scores, and three samples were counted for each group. (C) The histogram shows the rate of the GFP + cells in bone marrow. Three samples were counted for each group. (D) The survival curve of the mice (n=9 per group) tail-vein injected with Jurkat cells that were transduced with retroviruses expressing shRNAs targeting ARRB1, full-length ARRB1 or scrambled sequence expressing vector (scr). (E) CCK8 assay. The effect of ARRB1 overexpression or silencing on the proliferation of the T-ALL cell lines Jurkat, Molt4, and CCRF-CEM. “**” p
    Figure Legend Snippet: ARRB1 inhibits the tumor progression of human T-ALL cells. (A) GFP- and firefly luciferase-tagged Jurkat cells with ARRB1 overexpression (β1) or knockdown (sh-1 and sh-2) were tail-vein injected into irradiated NOD/SCID mice (n=5 per group). Twenty-one days after injection, bioluminescence images were obtained after administrating the mice D-Luciferin sodium salt. Subsequently, the mice were sacrificed, the spleens were spliced and stained with an anti-CD45RA antibody, and the bone marrow of the femurs was flushed out and subjected to anti-GFP immunostaining to assess the leukemia burden. Black scale bar, 500 μm; white scale bar, 100 μm. (B) The histogram shows the scores for the CD45RA + cells in the spleens. Image Pro Plus was used to calculate the scores, and three samples were counted for each group. (C) The histogram shows the rate of the GFP + cells in bone marrow. Three samples were counted for each group. (D) The survival curve of the mice (n=9 per group) tail-vein injected with Jurkat cells that were transduced with retroviruses expressing shRNAs targeting ARRB1, full-length ARRB1 or scrambled sequence expressing vector (scr). (E) CCK8 assay. The effect of ARRB1 overexpression or silencing on the proliferation of the T-ALL cell lines Jurkat, Molt4, and CCRF-CEM. “**” p

    Techniques Used: Luciferase, Over Expression, Injection, Irradiation, Mouse Assay, Staining, Immunostaining, Transduction, Expressing, Sequencing, Plasmid Preparation, CCK-8 Assay

    11) Product Images from "Potentiation of antileukemic therapies by the dual PI3K/PDK-1 inhibitor, BAG956: effects on BCR-ABL- and mutant FLT3-expressing cells"

    Article Title: Potentiation of antileukemic therapies by the dual PI3K/PDK-1 inhibitor, BAG956: effects on BCR-ABL- and mutant FLT3-expressing cells

    Journal: Blood

    doi: 10.1182/blood-2007-09-114454

    BAG956 inhibits proliferation of human leukemia cells. (A) BAG956 treatment (3-day) of Ba/F3, CCRF-CEM, Jurkat, THP-1, BV-173, KU812, MEG-01.(B) BAG956 treatment (4-day) of C1498, SUP-B15, KG-1, GDM-1. (C)BAG956 treatment (3-day) of Ba/F3 and Ba/F3.p210. (D) BAG956 treatment of primary AML patient bone marrow cells after 24 hours of treatment. (E) Left panel: Colony assay investigating effect of BAG956 on normal human bone marrow. Right panel: Colony assay investigating effect of BAG956 on primary murine bone marrow cells. (F) Colony assay investigating effect of BAG956 on primary AML patient bone marrow cells.
    Figure Legend Snippet: BAG956 inhibits proliferation of human leukemia cells. (A) BAG956 treatment (3-day) of Ba/F3, CCRF-CEM, Jurkat, THP-1, BV-173, KU812, MEG-01.(B) BAG956 treatment (4-day) of C1498, SUP-B15, KG-1, GDM-1. (C)BAG956 treatment (3-day) of Ba/F3 and Ba/F3.p210. (D) BAG956 treatment of primary AML patient bone marrow cells after 24 hours of treatment. (E) Left panel: Colony assay investigating effect of BAG956 on normal human bone marrow. Right panel: Colony assay investigating effect of BAG956 on primary murine bone marrow cells. (F) Colony assay investigating effect of BAG956 on primary AML patient bone marrow cells.

    Techniques Used: Colony Assay

    12) Product Images from "Matrine induced G0/G1 arrest and apoptosis in human acute T-cell lymphoblastic leukemia (T-ALL) cells"

    Article Title: Matrine induced G0/G1 arrest and apoptosis in human acute T-cell lymphoblastic leukemia (T-ALL) cells

    Journal: Bosnian Journal of Basic Medical Sciences

    doi: 10.17305/bjbms.2017.2457

    Hierarchical clustering of the RNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 49 RNAs, 24 were upregulated and 3 were downregulated and exhibited ≥2-fold change in expression relative to the untreated CCRF-CEM control cells. All experiments were performed in triplicate and Hs18s, GAPDH , and HPRT1 were used as housekeeping controls. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. CDKN1A ( p = 0.000159), IL6 ( p = 0.000011), KDR ( p = 0.001288), and VEGFC ( p = 0.000004) gene expressions were prominently upregulated, whereas BCL 2 ( p = 0.002893), CDKN 3 ( p = 0.000024), and E2F 1 ( p = 0.000128) gene expressions were downregulated in matrine-treated CCRF-CEM cells compared with untreated control CCRF-CEM cells.
    Figure Legend Snippet: Hierarchical clustering of the RNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 49 RNAs, 24 were upregulated and 3 were downregulated and exhibited ≥2-fold change in expression relative to the untreated CCRF-CEM control cells. All experiments were performed in triplicate and Hs18s, GAPDH , and HPRT1 were used as housekeeping controls. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. CDKN1A ( p = 0.000159), IL6 ( p = 0.000011), KDR ( p = 0.001288), and VEGFC ( p = 0.000004) gene expressions were prominently upregulated, whereas BCL 2 ( p = 0.002893), CDKN 3 ( p = 0.000024), and E2F 1 ( p = 0.000128) gene expressions were downregulated in matrine-treated CCRF-CEM cells compared with untreated control CCRF-CEM cells.

    Techniques Used: RNA Expression, Expressing

    Hierarchical clustering of the miRNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 44 miRNAs, 42 were downregulated and exhibited ≥2-fold change in expression relative to untreated control CCRF-CEM cells. All experiments were performed in triplicate and RNU6-2 was used as an endogenous control. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. Hsa-miR-376b-3p ( p = 0.008), hsa-miR-106b-3p ( p = 0.028), hsa-miR-20a-3p ( p = 0.014), hsa-miR-519a-3p ( p = 0.00534), and hsa-miR-204-5p ( p = 0.001) expression levels were significantly decreased in the matrine-treated compared to untreated control cells.
    Figure Legend Snippet: Hierarchical clustering of the miRNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 44 miRNAs, 42 were downregulated and exhibited ≥2-fold change in expression relative to untreated control CCRF-CEM cells. All experiments were performed in triplicate and RNU6-2 was used as an endogenous control. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. Hsa-miR-376b-3p ( p = 0.008), hsa-miR-106b-3p ( p = 0.028), hsa-miR-20a-3p ( p = 0.014), hsa-miR-519a-3p ( p = 0.00534), and hsa-miR-204-5p ( p = 0.001) expression levels were significantly decreased in the matrine-treated compared to untreated control cells.

    Techniques Used: Expressing

    13) Product Images from "Extensive Remodeling of the Immune Microenvironment in B-cell Acute Lymphoblastic Leukemia"

    Article Title: Extensive Remodeling of the Immune Microenvironment in B-cell Acute Lymphoblastic Leukemia

    Journal: Cancer cell

    doi: 10.1016/j.ccell.2020.04.015

    Non-classical Monocyte Abundance Predicts Inferior Overall Survival in Pediatric B-ALL Cases. A-B , Kaplan-Meier analysis of newly-diagnosed pediatric B-ALL patient (A) overall survival (OS) and (B) relapse-free survival (RFS). Patients were separated on the basis of absolute monocytosis at disease presentation, with two cohorts absolute monocyte counts (AMC) > 1000 cells/μL and AMC ≤ 1000 cells/μL. Number of patients indicated (n). Log-rank tests of equality were used to compare the differences in survival rates. C-D, Kaplan-Meier analysis of adolescent/young adult (AYA) human B-ALL patient (C) overall survival and (D) ). Monocyte High patients represent the upper-quartile of monocyte scores, and Monocyte Low represents the lower-quartile. Number of patients indicated (n).
    Figure Legend Snippet: Non-classical Monocyte Abundance Predicts Inferior Overall Survival in Pediatric B-ALL Cases. A-B , Kaplan-Meier analysis of newly-diagnosed pediatric B-ALL patient (A) overall survival (OS) and (B) relapse-free survival (RFS). Patients were separated on the basis of absolute monocytosis at disease presentation, with two cohorts absolute monocyte counts (AMC) > 1000 cells/μL and AMC ≤ 1000 cells/μL. Number of patients indicated (n). Log-rank tests of equality were used to compare the differences in survival rates. C-D, Kaplan-Meier analysis of adolescent/young adult (AYA) human B-ALL patient (C) overall survival and (D) ). Monocyte High patients represent the upper-quartile of monocyte scores, and Monocyte Low represents the lower-quartile. Number of patients indicated (n).

    Techniques Used:

    14) Product Images from "131I anti-CD45 radioimmunotherapy effectively targets and treats T-cell non-Hodgkin lymphoma"

    Article Title: 131I anti-CD45 radioimmunotherapy effectively targets and treats T-cell non-Hodgkin lymphoma

    Journal: Blood

    doi: 10.1182/blood-2009-02-205476

    Biodistribution of 131 I-BC8 (anti-CD45) and 125 I-BHV-1 (control) in a human T-NHL xenograft model . Biodistributions quantified as percentage injected radioiodine dose/g tissue (%ID/g) of 131 I-BC8 (anti-CD45, ■) and 125 I-BHV-1 (control, ) in mice with CCRF-CEM (A,B) and Karpas 299 (C,D) xenografts after 24 and 48 hours.
    Figure Legend Snippet: Biodistribution of 131 I-BC8 (anti-CD45) and 125 I-BHV-1 (control) in a human T-NHL xenograft model . Biodistributions quantified as percentage injected radioiodine dose/g tissue (%ID/g) of 131 I-BC8 (anti-CD45, ■) and 125 I-BHV-1 (control, ) in mice with CCRF-CEM (A,B) and Karpas 299 (C,D) xenografts after 24 and 48 hours.

    Techniques Used: Injection, Mouse Assay

    Tumor-to-normal organ ratios of retained radioactivity following targeting of human T-NHL xenografts with 131 I-BC8 (anti-CD45) and I-125-BHV-1 (control) . Tumor-to-normal organ ratios of percentage injected radioiodine/g tissue of 131 I-BC8 (anti-CD45, ■) and 125 I-BHV-1 (control, ) in mice with CCRF-CEM (A,B) and Karpas 299 (C,D) xenografts after 24 and 48 hours.
    Figure Legend Snippet: Tumor-to-normal organ ratios of retained radioactivity following targeting of human T-NHL xenografts with 131 I-BC8 (anti-CD45) and I-125-BHV-1 (control) . Tumor-to-normal organ ratios of percentage injected radioiodine/g tissue of 131 I-BC8 (anti-CD45, ■) and 125 I-BHV-1 (control, ) in mice with CCRF-CEM (A,B) and Karpas 299 (C,D) xenografts after 24 and 48 hours.

    Techniques Used: Radioactivity, Injection, Mouse Assay

    15) Product Images from "Regulation of PI3K signaling in T cell acute lymphoblastic leukemia: a novel PTEN/Ikaros/miR-26b mechanism reveals a critical targetable role for PIK3CD"

    Article Title: Regulation of PI3K signaling in T cell acute lymphoblastic leukemia: a novel PTEN/Ikaros/miR-26b mechanism reveals a critical targetable role for PIK3CD

    Journal: Leukemia

    doi: 10.1038/leu.2017.80

    Inhibition of PIK3CD by CAL-101 or shRNAs reduced the growth of T-ALL cells A: T-ALL cell lines were treated with 1–40 μM of CAL-101, and cell inhibition ratios were measured at several time points. B: PI3K p110δ protein levels were assessed by Western blot in T-ALL cells infected with control vector or overexpressing shRNAs for PIK3CD . C: In CCRF-CEM and KOPT-K1 T-ALL cell lines, cell proliferation decreased and apoptosis increased after the knockdown of PIK3CD by shRNA1 or shRNA2.
    Figure Legend Snippet: Inhibition of PIK3CD by CAL-101 or shRNAs reduced the growth of T-ALL cells A: T-ALL cell lines were treated with 1–40 μM of CAL-101, and cell inhibition ratios were measured at several time points. B: PI3K p110δ protein levels were assessed by Western blot in T-ALL cells infected with control vector or overexpressing shRNAs for PIK3CD . C: In CCRF-CEM and KOPT-K1 T-ALL cell lines, cell proliferation decreased and apoptosis increased after the knockdown of PIK3CD by shRNA1 or shRNA2.

    Techniques Used: Inhibition, Western Blot, Infection, Plasmid Preparation

    miR-26b inhibits the growth of T-ALL cells in vivo A: Tumor burden was monitored and assessed in a xenograft T-ALL mouse model by bioluminescence imaging at the indicated time points. B: Tumor burden of peripheral blood was detected by flow cytometry (GFP and hCD45 staining) and the phospho-AKT level of CCRF-CEM-FFluc cells was measured by intracellular staining flow cytometry on day 15. C: Kaplan-Meier survival curve (P=0.0031).
    Figure Legend Snippet: miR-26b inhibits the growth of T-ALL cells in vivo A: Tumor burden was monitored and assessed in a xenograft T-ALL mouse model by bioluminescence imaging at the indicated time points. B: Tumor burden of peripheral blood was detected by flow cytometry (GFP and hCD45 staining) and the phospho-AKT level of CCRF-CEM-FFluc cells was measured by intracellular staining flow cytometry on day 15. C: Kaplan-Meier survival curve (P=0.0031).

    Techniques Used: In Vivo, Imaging, Flow Cytometry, Cytometry, Staining

    16) Product Images from "Fbxo7 promotes Cdk6 activity to inhibit PFKP and glycolysis in T cells"

    Article Title: Fbxo7 promotes Cdk6 activity to inhibit PFKP and glycolysis in T cells

    Journal: bioRxiv

    doi: 10.1101/2021.11.05.467417

    Fbxo7 knockdown in T-ALL cells reduces the proportion of inactive monomer/dimer PFKP and promotes glycolysis. (A) Lysates from cells expressing a control or Fbxo7 shRNA, and with Fbxo7 over-expression, were analysed by immunoblot and quantified (CCRF-CEM n=4, HEK293T n=3). (B) Representative immunoblot of PFKP half-life in CCRF-CEM cells expressing a control or Fbxo7 shRNA and treated with cycloheximide for up to 24 hours (n=2). (C) Cells were treated with DMSO or 10 μM MG132 for 4 hours and lysed. Proteins were resolved by SDS-PAGE to immunoblot for PFKP, and levels were quantified (CCRF-CEM n=2, HEK293T n=3). (D) Lysates from CCRF-CEM cells with control or Fbxo7 shRNA were passed over a 200 kDa molecular weight cut-off filter to separate PFKP monomers (86 kDa) and dimers (172 kDa) from tetramers (344 kDa). AMP and citrate were added to lysates as controls to respectively promote or dissociate PFKP tetramers. Total lysates and
    Figure Legend Snippet: Fbxo7 knockdown in T-ALL cells reduces the proportion of inactive monomer/dimer PFKP and promotes glycolysis. (A) Lysates from cells expressing a control or Fbxo7 shRNA, and with Fbxo7 over-expression, were analysed by immunoblot and quantified (CCRF-CEM n=4, HEK293T n=3). (B) Representative immunoblot of PFKP half-life in CCRF-CEM cells expressing a control or Fbxo7 shRNA and treated with cycloheximide for up to 24 hours (n=2). (C) Cells were treated with DMSO or 10 μM MG132 for 4 hours and lysed. Proteins were resolved by SDS-PAGE to immunoblot for PFKP, and levels were quantified (CCRF-CEM n=2, HEK293T n=3). (D) Lysates from CCRF-CEM cells with control or Fbxo7 shRNA were passed over a 200 kDa molecular weight cut-off filter to separate PFKP monomers (86 kDa) and dimers (172 kDa) from tetramers (344 kDa). AMP and citrate were added to lysates as controls to respectively promote or dissociate PFKP tetramers. Total lysates and

    Techniques Used: Expressing, shRNA, Over Expression, SDS Page, Molecular Weight

    Fbxo7 ubiquitinates PFKP. (A) Fbxo7 immunoprecipitation from CCRF-CEM cells, showing co-immunoprecipitation of PFKP (n=3). (B) Schematic of Fbxo7 constructs used to make SCF ligases or for in vivo ubiquitination assays. All contain an N-terminal FLAG tag (not shown). Ubl, ubiquitin-like domain; Cdk6, Cdk6-binding domain; FP, Fbxo7-PI31 dimerization domain; PRR, proline rich region. (C) FLAG-Fbxo7 constructs were transfected into HEK293T cells alongside Skp1, Cullin1 (Cul1) and myc-Rbx1. SCF complexes were isolated by FLAG immunoprecipitation, and the presence of the other SCF components was confirmed by immunoblot. (D) In vitro ubiquitination assay of SCF Fbxo7 complexes in C, together with HA-PFKP and a ubiquitin mix (ubiquitin buffer, UBE1, UbcH5a and ATP) (n=2). (E) In vivo ubiquitination assay of Fbxo7 constructs with PFKP. Constructs were over-expressed in HEK293T cells stably expressing a control or Fbxo7 shRNA. Ubiquitinated proteins were isolated using a cobalt-NTA affinity resin (Co-NTA) to the His-tag on ubiquitin. Immunoblot for PFKP shows the degree of ubiquitination following expression of each Fbxo7 construct (n=3).
    Figure Legend Snippet: Fbxo7 ubiquitinates PFKP. (A) Fbxo7 immunoprecipitation from CCRF-CEM cells, showing co-immunoprecipitation of PFKP (n=3). (B) Schematic of Fbxo7 constructs used to make SCF ligases or for in vivo ubiquitination assays. All contain an N-terminal FLAG tag (not shown). Ubl, ubiquitin-like domain; Cdk6, Cdk6-binding domain; FP, Fbxo7-PI31 dimerization domain; PRR, proline rich region. (C) FLAG-Fbxo7 constructs were transfected into HEK293T cells alongside Skp1, Cullin1 (Cul1) and myc-Rbx1. SCF complexes were isolated by FLAG immunoprecipitation, and the presence of the other SCF components was confirmed by immunoblot. (D) In vitro ubiquitination assay of SCF Fbxo7 complexes in C, together with HA-PFKP and a ubiquitin mix (ubiquitin buffer, UBE1, UbcH5a and ATP) (n=2). (E) In vivo ubiquitination assay of Fbxo7 constructs with PFKP. Constructs were over-expressed in HEK293T cells stably expressing a control or Fbxo7 shRNA. Ubiquitinated proteins were isolated using a cobalt-NTA affinity resin (Co-NTA) to the His-tag on ubiquitin. Immunoblot for PFKP shows the degree of ubiquitination following expression of each Fbxo7 construct (n=3).

    Techniques Used: Immunoprecipitation, Construct, In Vivo, FLAG-tag, Binding Assay, Transfection, Isolation, In Vitro, Ubiquitin Assay, Stable Transfection, Expressing, shRNA

    17) Product Images from "Metformin Induces Apoptosis through AMPK-Dependent Inhibition of UPR Signaling in ALL Lymphoblasts"

    Article Title: Metformin Induces Apoptosis through AMPK-Dependent Inhibition of UPR Signaling in ALL Lymphoblasts

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0074420

    Metformin activates AMPK, Akt, and UPR signaling pathway proteins in ALL primary and cell line models. A ) Western blot analysis of proteins associated with AMPK, and Akt/mTOR signaling pathways in CCRF-CEM and NALM6 cells treated with metformin (MET, 2.5 and 5.0 mM) for 48 h. The density value of each band was normalized to β-actin level and expressed relative to control (shown as fold induction). B ) Immunoblotting of UPR signaling factors in CCRF-CEM and NALM6 cells treated with metformin (MET, 2.5 and 5.0 mM) for 48 h. C ) Western blots of AMPK, Akt/mTOR and UPR signaling proteins in representative sample of primary T- and Bp-ALL cells treated with metformin (MET, 10 mM) for 24 h. D ) Western blot analysis of GRP78 expression in CCRF-CEM and NALM6 cells treated with metformin (MET, 10mM) and tunicamycin (TUN, 2.5 µg/ml for NALM6; 5.0 µg/ml for CCRF-CEM), either alone or in combination for 48 h.
    Figure Legend Snippet: Metformin activates AMPK, Akt, and UPR signaling pathway proteins in ALL primary and cell line models. A ) Western blot analysis of proteins associated with AMPK, and Akt/mTOR signaling pathways in CCRF-CEM and NALM6 cells treated with metformin (MET, 2.5 and 5.0 mM) for 48 h. The density value of each band was normalized to β-actin level and expressed relative to control (shown as fold induction). B ) Immunoblotting of UPR signaling factors in CCRF-CEM and NALM6 cells treated with metformin (MET, 2.5 and 5.0 mM) for 48 h. C ) Western blots of AMPK, Akt/mTOR and UPR signaling proteins in representative sample of primary T- and Bp-ALL cells treated with metformin (MET, 10 mM) for 24 h. D ) Western blot analysis of GRP78 expression in CCRF-CEM and NALM6 cells treated with metformin (MET, 10mM) and tunicamycin (TUN, 2.5 µg/ml for NALM6; 5.0 µg/ml for CCRF-CEM), either alone or in combination for 48 h.

    Techniques Used: Western Blot, Expressing

    Metformin induces expression of PIM-2 in ALL cells. Western blot analysis of PIM-2, p-BAD (S112) and p-AMPK (T172) expression in CCRF-CEM and NALM6 cells treated with metformin (MET, 5 and 10 mM) for 72 h at 37°C.
    Figure Legend Snippet: Metformin induces expression of PIM-2 in ALL cells. Western blot analysis of PIM-2, p-BAD (S112) and p-AMPK (T172) expression in CCRF-CEM and NALM6 cells treated with metformin (MET, 5 and 10 mM) for 72 h at 37°C.

    Techniques Used: Expressing, Western Blot

    Metformin induces cell growth arrest and apoptosis in ALL cell lines. Growth inhibition ( A ) and apoptosis ( B ) in CCRF-CEM and NALM6 cells treated with metformin (MET, 1, 2, and 5 mM) for 48 h. Apoptosis ( C ) in T-ALL (CCRF-CEM, Jurkat, and primary T-ALL) and Bp-ALL (NALM6, REH, and primary Bp-ALL) cells treated with metformin (MET, 5 mM) for 48 h. Growth inhibition was expressed relative to control values (mean ±SEM, n = 3). * and # denote p
    Figure Legend Snippet: Metformin induces cell growth arrest and apoptosis in ALL cell lines. Growth inhibition ( A ) and apoptosis ( B ) in CCRF-CEM and NALM6 cells treated with metformin (MET, 1, 2, and 5 mM) for 48 h. Apoptosis ( C ) in T-ALL (CCRF-CEM, Jurkat, and primary T-ALL) and Bp-ALL (NALM6, REH, and primary Bp-ALL) cells treated with metformin (MET, 5 mM) for 48 h. Growth inhibition was expressed relative to control values (mean ±SEM, n = 3). * and # denote p

    Techniques Used: Inhibition

    Inhibition of PIM-2 and Akt kinases synergistically sensitizes ALL cells to metformin. A ) Cell death in CCRF-CEM and NALM6 cells treated with metformin (MET, 4 mM) and the PIM-1/2 kinase inhibitor V (PKI; 80 µM), either alone or in combination for 72 h at 37°C. The CI values of 0.27 and 0.28 indicate synergism. B ) Immunoblotting of p-ACC (S79), GRP78, and PIM-2 expression in the CCRF-CEM and NALM6 cells treated with MET plus PKI described in ( A ). C ) Cell death in NALM6 cells treated with metformin (MET, 5.0 mM) and Akt inhibitor X (AIX; 5 µM) or perifosine (PER; 6 µM), either alone or in combination for 72 h at 37°C. CI values of 0.19 (MET + AIX) and 0.21 (MET + PER) indicate synergism. The cell death values were expressed as a percentage (%) of cells in the population (mean ±SEM, n = 3). D ) Immunoblotting of AMPK/ACC, Akt/mTOR, and UPR signaling pathway proteins in the NALM6 cells treated with MET (5.0 mM) plus AIX (5 µM) described in ( C ).
    Figure Legend Snippet: Inhibition of PIM-2 and Akt kinases synergistically sensitizes ALL cells to metformin. A ) Cell death in CCRF-CEM and NALM6 cells treated with metformin (MET, 4 mM) and the PIM-1/2 kinase inhibitor V (PKI; 80 µM), either alone or in combination for 72 h at 37°C. The CI values of 0.27 and 0.28 indicate synergism. B ) Immunoblotting of p-ACC (S79), GRP78, and PIM-2 expression in the CCRF-CEM and NALM6 cells treated with MET plus PKI described in ( A ). C ) Cell death in NALM6 cells treated with metformin (MET, 5.0 mM) and Akt inhibitor X (AIX; 5 µM) or perifosine (PER; 6 µM), either alone or in combination for 72 h at 37°C. CI values of 0.19 (MET + AIX) and 0.21 (MET + PER) indicate synergism. The cell death values were expressed as a percentage (%) of cells in the population (mean ±SEM, n = 3). D ) Immunoblotting of AMPK/ACC, Akt/mTOR, and UPR signaling pathway proteins in the NALM6 cells treated with MET (5.0 mM) plus AIX (5 µM) described in ( C ).

    Techniques Used: Inhibition, Expressing

    Inhibition of mTOR-dependent protein synthesis reverses metformin-induced cell death. A ) Apoptosis in CCRF-CEM cells expressing either scramble shRNA (shCTRL) or shRNA against AMPKα1 (shAMPK) treated with metformin (MET, 10 mM) for 48 h. B ) Immunoblotting of AMPK, Akt/mTOR, and ER stress/UPR signaling pathway proteins in the cells described in ( A ). C ) Cell death ( upper panel ) in CCRF-CEM and NALM6 cells treated with metformin (MET, 5 and 10 mM) and rapamycin (RAPA; 0.1 µg/mL), either alone or in combination for 48 h. A statistical value of p
    Figure Legend Snippet: Inhibition of mTOR-dependent protein synthesis reverses metformin-induced cell death. A ) Apoptosis in CCRF-CEM cells expressing either scramble shRNA (shCTRL) or shRNA against AMPKα1 (shAMPK) treated with metformin (MET, 10 mM) for 48 h. B ) Immunoblotting of AMPK, Akt/mTOR, and ER stress/UPR signaling pathway proteins in the cells described in ( A ). C ) Cell death ( upper panel ) in CCRF-CEM and NALM6 cells treated with metformin (MET, 5 and 10 mM) and rapamycin (RAPA; 0.1 µg/mL), either alone or in combination for 48 h. A statistical value of p

    Techniques Used: Inhibition, Expressing, shRNA

    18) Product Images from "Niclosamide suppresses T-cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy"

    Article Title: Niclosamide suppresses T-cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy

    Journal: Oncology Reports

    doi: 10.3892/or.2021.8241

    Niclosamide induces T-ALL cell autophagy in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of LC3B, p62 and ATG5 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P
    Figure Legend Snippet: Niclosamide induces T-ALL cell autophagy in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of LC3B, p62 and ATG5 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P

    Techniques Used: Expressing, Western Blot

    Niclosamide induces T-ALL cell apoptosis in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of Bcl-2, cleaved caspase-3 and caspase-3 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P
    Figure Legend Snippet: Niclosamide induces T-ALL cell apoptosis in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of Bcl-2, cleaved caspase-3 and caspase-3 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P

    Techniques Used: Expressing, Western Blot

    Niclosamide induces apoptosis in T-ALL cells. Jurkat and CCRF-CEM cells were treated with DMSO (vehicle control), and niclosamide for 24 h. (A) Flow cytometric analysis of apoptosis was evaluated by using Annexin V-FITC and PI double staining at 24 h posterior to the treatment. (B) Quantitative analysis of the apoptotic cells from A. The results are expressed as mean ± SEM. ****P
    Figure Legend Snippet: Niclosamide induces apoptosis in T-ALL cells. Jurkat and CCRF-CEM cells were treated with DMSO (vehicle control), and niclosamide for 24 h. (A) Flow cytometric analysis of apoptosis was evaluated by using Annexin V-FITC and PI double staining at 24 h posterior to the treatment. (B) Quantitative analysis of the apoptotic cells from A. The results are expressed as mean ± SEM. ****P

    Techniques Used: Double Staining

    Niclosamide effectively inhibits the viability of T-ALL cells in a dose- and time-dependent manner. Human T-ALL cells were treated with niclosamide for 24 h. Cell viability and proliferation was measured by MTT assays and flow cytometry of Ki-67 staining, respectively. MTT assays showed that niclosamide inhibited the proliferation of (A) Jurkat and (B) CCRF-CEM cells dose-dependently. (C) Jurkat and (D) CCRF-CEM cells were treated with niclosamide for 24, 48 and 72 h. MTT assays showed that niclosamide inhibited the proliferation of Jurkat and CCRF-CEM cells time-dependently. MFI of Ki-67 were examined by flow cytometry after incubation of (E) Jurkat and (F) CCRF-CEM cells treated with different doses of niclosamide for 24 h. Niclosamide treatment effectively inhibited the proliferation of T-ALL cells dose-dependently. The results are expressed as mean ± SEM. *P
    Figure Legend Snippet: Niclosamide effectively inhibits the viability of T-ALL cells in a dose- and time-dependent manner. Human T-ALL cells were treated with niclosamide for 24 h. Cell viability and proliferation was measured by MTT assays and flow cytometry of Ki-67 staining, respectively. MTT assays showed that niclosamide inhibited the proliferation of (A) Jurkat and (B) CCRF-CEM cells dose-dependently. (C) Jurkat and (D) CCRF-CEM cells were treated with niclosamide for 24, 48 and 72 h. MTT assays showed that niclosamide inhibited the proliferation of Jurkat and CCRF-CEM cells time-dependently. MFI of Ki-67 were examined by flow cytometry after incubation of (E) Jurkat and (F) CCRF-CEM cells treated with different doses of niclosamide for 24 h. Niclosamide treatment effectively inhibited the proliferation of T-ALL cells dose-dependently. The results are expressed as mean ± SEM. *P

    Techniques Used: MTT Assay, Flow Cytometry, Staining, Incubation

    19) Product Images from "Metformin Induces Cell Cycle Arrest and Apoptosis in Drug-Resistant Leukemia Cells"

    Article Title: Metformin Induces Cell Cycle Arrest and Apoptosis in Drug-Resistant Leukemia Cells

    Journal: Leukemia Research and Treatment

    doi: 10.1155/2015/516460

    Metformin induces mitochondrial perturbations. CEM and 10E 1 -CEM cells were exposed to metformin (10 mM) for 48 h and then stained with DiOC 6 (3)/PI. The Δ ψ m was determined as DiOC 3 (6) emitted fluorescence (black: control cells, red: metformin-treated cells). Fluorescence by CEM cells treated with 4-HPR has been shown as positive control (CEM CTRL+). In all cases, differences of mean fluorescence intensity of metformin versus control ( n = 10.000 cells analyzed/assay) are statistically significant ( P
    Figure Legend Snippet: Metformin induces mitochondrial perturbations. CEM and 10E 1 -CEM cells were exposed to metformin (10 mM) for 48 h and then stained with DiOC 6 (3)/PI. The Δ ψ m was determined as DiOC 3 (6) emitted fluorescence (black: control cells, red: metformin-treated cells). Fluorescence by CEM cells treated with 4-HPR has been shown as positive control (CEM CTRL+). In all cases, differences of mean fluorescence intensity of metformin versus control ( n = 10.000 cells analyzed/assay) are statistically significant ( P

    Techniques Used: Staining, Fluorescence, Positive Control

    20) Product Images from "Glucocorticoid Resistant Pediatric Acute Lymphoblastic Leukemia Samples Display Altered Splicing Profile and Vulnerability to Spliceosome Modulation"

    Article Title: Glucocorticoid Resistant Pediatric Acute Lymphoblastic Leukemia Samples Display Altered Splicing Profile and Vulnerability to Spliceosome Modulation

    Journal: Cancers

    doi: 10.3390/cancers12030723

    Response of (GC-resistant) T-cell ALL cells to splicing modulation. The figure illustrates the effects of splicing modulation on T-ALL cell lines and primary childhood samples as well as non-malignant specimens. ( A ) Response to Plad-B of GC-sensitive CCRF-CEM-WT cells as well as its GC-resistant sublines: CEM-R30dm, CEM-R5 and CEM-R5C3 in a 72 h MTT assay. The plot depicts the mean ± SD of at least 3 independent experiments. ( B , C ) Time-dependent inhibition of proliferation ( B ) and cell cycle arrest ( C ) induced by treatment with 4 nM Plad-B in CEM-WT and CEM-R30dm. The panel depicts the mean ± SD of 2 independent experiments. T-test was used for ( B ); asterisks in ( B , C ) indicate statistical significance ( p
    Figure Legend Snippet: Response of (GC-resistant) T-cell ALL cells to splicing modulation. The figure illustrates the effects of splicing modulation on T-ALL cell lines and primary childhood samples as well as non-malignant specimens. ( A ) Response to Plad-B of GC-sensitive CCRF-CEM-WT cells as well as its GC-resistant sublines: CEM-R30dm, CEM-R5 and CEM-R5C3 in a 72 h MTT assay. The plot depicts the mean ± SD of at least 3 independent experiments. ( B , C ) Time-dependent inhibition of proliferation ( B ) and cell cycle arrest ( C ) induced by treatment with 4 nM Plad-B in CEM-WT and CEM-R30dm. The panel depicts the mean ± SD of 2 independent experiments. T-test was used for ( B ); asterisks in ( B , C ) indicate statistical significance ( p

    Techniques Used: MTT Assay, Inhibition

    21) Product Images from "Staphylococcal Superantigen-like 10 Inhibits CXCL12-Induced Human Tumor Cell Migration 1"

    Article Title: Staphylococcal Superantigen-like 10 Inhibits CXCL12-Induced Human Tumor Cell Migration 1

    Journal:

    doi:

    SSL10 binds CXCR4. (A) CXCR4-expressing Jurkat T-ALL cells were incubated with or without 10 µ g/ml SSL10 for 30 minutes on ice. After washing, cells were stained with anti-CXCR4 mAb and detected with FITC-conjugated goat antimouse IgG. Continuous
    Figure Legend Snippet: SSL10 binds CXCR4. (A) CXCR4-expressing Jurkat T-ALL cells were incubated with or without 10 µ g/ml SSL10 for 30 minutes on ice. After washing, cells were stained with anti-CXCR4 mAb and detected with FITC-conjugated goat antimouse IgG. Continuous

    Techniques Used: Expressing, Incubation, Staining

    22) Product Images from "Deciphering intratumoral heterogeneity using integrated clonal tracking and single-cell transcriptome analyses"

    Article Title: Deciphering intratumoral heterogeneity using integrated clonal tracking and single-cell transcriptome analyses

    Journal: Nature Communications

    doi: 10.1038/s41467-021-26771-1

    Relapsed leukemia cells generate greater clonal dominance in the PDX model than chemotherapy-naïve cells from the same patients. a Human B-ALL cells acquired from two patients at distinct disease stages (chemotherapy naïve and chemotherapy relapsed) were genetically labeled with DNA barcodes and transplanted into irradiated immunocompromised mice. Leukemia progression was monitored through peripheral blood analysis. b Human chimerism of the mouse peripheral blood following transplantation of diagnostic (naïve) and relapsed leukemia cells from the same patients. Each line depicts data from one mouse. c Number of unique DNA barcodes detected in the peripheral blood. Each line depicts data from one mouse. ** P
    Figure Legend Snippet: Relapsed leukemia cells generate greater clonal dominance in the PDX model than chemotherapy-naïve cells from the same patients. a Human B-ALL cells acquired from two patients at distinct disease stages (chemotherapy naïve and chemotherapy relapsed) were genetically labeled with DNA barcodes and transplanted into irradiated immunocompromised mice. Leukemia progression was monitored through peripheral blood analysis. b Human chimerism of the mouse peripheral blood following transplantation of diagnostic (naïve) and relapsed leukemia cells from the same patients. Each line depicts data from one mouse. c Number of unique DNA barcodes detected in the peripheral blood. Each line depicts data from one mouse. ** P

    Techniques Used: Labeling, Irradiation, Mouse Assay, Transplantation Assay, Diagnostic Assay

    23) Product Images from "A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions"

    Article Title: A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2018.09.025

    The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p
    Figure Legend Snippet: The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p

    Techniques Used: Infection, Immunostaining

    24) Product Images from "Diphtheria Toxin/Human B-Cell Activating Factor Fusion Protein Kills Human Acute Lymphoblastic Leukemia BALL-1 Cells: An Experimental Study"

    Article Title: Diphtheria Toxin/Human B-Cell Activating Factor Fusion Protein Kills Human Acute Lymphoblastic Leukemia BALL-1 Cells: An Experimental Study

    Journal: Chinese Journal of Cancer Research

    doi: 10.1007/s11670-012-0238-0

    mRNA levels of BAFF receptors in BALL-1, Hmy2.CIR and U937 cells assessed by real-time PCR. The mRNA levels were normalized with GAPDH. BALL-R relative expression levels in BALL-1, Hmy2.CIR and U937 cells were respectively 0.7, 1.0, and 0/undetectable,
    Figure Legend Snippet: mRNA levels of BAFF receptors in BALL-1, Hmy2.CIR and U937 cells assessed by real-time PCR. The mRNA levels were normalized with GAPDH. BALL-R relative expression levels in BALL-1, Hmy2.CIR and U937 cells were respectively 0.7, 1.0, and 0/undetectable,

    Techniques Used: Real-time Polymerase Chain Reaction, Expressing

    25) Product Images from "Real-time RT-PCR analysis of mRNA decay: half-life of Beta-actin mRNA in human leukemia CCRF-CEM and Nalm-6 cell lines"

    Article Title: Real-time RT-PCR analysis of mRNA decay: half-life of Beta-actin mRNA in human leukemia CCRF-CEM and Nalm-6 cell lines

    Journal: Cancer Cell International

    doi: 10.1186/1475-2867-2-1

    Half-life of β-actin mRNA in Nalm-6 and CCRF-CEM cells. The CCRF-CEM cells were treated with 5 μM (squares) or 1 μM (circles) Act-D for various times to block mRNA synthesis. Similarly, the Nalm6 cells were treated with 1 μM (lozenges) or 0.5 μM (triangles) Act-D. Total RNA, cDNA, and Real-Time PCR amplification were performed as described in the text. The values represent the mean (±) the standard deviation (SD) of the β-actin RNA copy number per μg of total RNA from three independent experiments. Triplicate determinations were averaged at each data-point. The inset shows the calculated half-life for the β-actin mRNA in each cell line for each treatment.
    Figure Legend Snippet: Half-life of β-actin mRNA in Nalm-6 and CCRF-CEM cells. The CCRF-CEM cells were treated with 5 μM (squares) or 1 μM (circles) Act-D for various times to block mRNA synthesis. Similarly, the Nalm6 cells were treated with 1 μM (lozenges) or 0.5 μM (triangles) Act-D. Total RNA, cDNA, and Real-Time PCR amplification were performed as described in the text. The values represent the mean (±) the standard deviation (SD) of the β-actin RNA copy number per μg of total RNA from three independent experiments. Triplicate determinations were averaged at each data-point. The inset shows the calculated half-life for the β-actin mRNA in each cell line for each treatment.

    Techniques Used: Activated Clotting Time Assay, Blocking Assay, Real-time Polymerase Chain Reaction, Amplification, Standard Deviation

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    ATCC human t all cell lines jurkat
    The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in <t>T-ALL</t> Cells (A) Human T-ALL cell lines <t>Jurkat</t> (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p
    Human T All Cell Lines Jurkat, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions

    doi: 10.1016/j.omtn.2018.09.025

    Figure Lengend Snippet: The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p

    Article Snippet: Cell Culture and Chemicals HEK293T, human breast cancer cell lines SKBR3 and MCF7, and human T-ALL cell lines Jurkat and CCRF-CEM were obtained from American Type Culture Collection (ATCC, Manassas, VA).

    Techniques: Infection, Immunostaining

    Glutathione synthesis is partially involved in adipocyte protection of ALL cells ( A ) Intracellular GSH quantification in 3T3-L1 adipocytes ( n = 3). Viable cell number of BV173 and Nalm6 cells treated with DNR (100 and 200 nM, respectively) while co-cultured with 3T3-L1 ( B ) or ChubS7 ( C ) adipocytes that were pre-treated with 20 mM BSO for 24 hours ( n = 8–10). ( D ) Viable cell number of BV173 and Nalm6 cells treated with DNR while co-cultured with 3T3-L1 adipocytes that were pre-treated with 250 nM AUR for 24 hours ( n = 3).* p

    Journal: Oncotarget

    Article Title: Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response

    doi: 10.18632/oncotarget.12246

    Figure Lengend Snippet: Glutathione synthesis is partially involved in adipocyte protection of ALL cells ( A ) Intracellular GSH quantification in 3T3-L1 adipocytes ( n = 3). Viable cell number of BV173 and Nalm6 cells treated with DNR (100 and 200 nM, respectively) while co-cultured with 3T3-L1 ( B ) or ChubS7 ( C ) adipocytes that were pre-treated with 20 mM BSO for 24 hours ( n = 8–10). ( D ) Viable cell number of BV173 and Nalm6 cells treated with DNR while co-cultured with 3T3-L1 adipocytes that were pre-treated with 250 nM AUR for 24 hours ( n = 3).* p

    Article Snippet: Cell culture All human ALL cell lines (BV173, RS4;11, and Nalm6) and murine pre-adipocyte 3T3-L1 were from ATCC.

    Techniques: Cell Culture

    Adipocytes protect ALL cells from oxidative stress ( A ) Measurement of % ROS high population in Nalm6 cells treated with DNR for 6 hours. % ROS high based on gates defined by cells without DNR treatment. Adipo condition is significantly different than both Fibro and No Feeder by repeated measure ANOVA ( p

    Journal: Oncotarget

    Article Title: Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response

    doi: 10.18632/oncotarget.12246

    Figure Lengend Snippet: Adipocytes protect ALL cells from oxidative stress ( A ) Measurement of % ROS high population in Nalm6 cells treated with DNR for 6 hours. % ROS high based on gates defined by cells without DNR treatment. Adipo condition is significantly different than both Fibro and No Feeder by repeated measure ANOVA ( p

    Article Snippet: Cell culture All human ALL cell lines (BV173, RS4;11, and Nalm6) and murine pre-adipocyte 3T3-L1 were from ATCC.

    Techniques:

    ALL cells induce oxidative stress in adipocytes ( A ) Representative fluorescent confocal microscopy images of 3T3-L1 adipocytes alone, with ALL in TransWells, or treated with 20 mM BSO for 48 hours. Top: DCF (green) only, bottom: DIC images. ( B ) Quantification of fluorescence (FITC) from 3 images similar to A. *indicate t -tests on log-transformed pixel counts. ( C ) 3T3-L1 gene expression by qPCR with (gray bar) and without (white bar) 8093 cells; n = 3. ( D ) Western blot of HO-1 expression in 3T3-L1 adipocytes exposed to DNR, ALL, or both. GAPDH was used as loading control. E. GSH levels measured in media after conditioning with BV173 ALL cells, 3T3-L1 adipocytes, or both, for 48 hours. * P

    Journal: Oncotarget

    Article Title: Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response

    doi: 10.18632/oncotarget.12246

    Figure Lengend Snippet: ALL cells induce oxidative stress in adipocytes ( A ) Representative fluorescent confocal microscopy images of 3T3-L1 adipocytes alone, with ALL in TransWells, or treated with 20 mM BSO for 48 hours. Top: DCF (green) only, bottom: DIC images. ( B ) Quantification of fluorescence (FITC) from 3 images similar to A. *indicate t -tests on log-transformed pixel counts. ( C ) 3T3-L1 gene expression by qPCR with (gray bar) and without (white bar) 8093 cells; n = 3. ( D ) Western blot of HO-1 expression in 3T3-L1 adipocytes exposed to DNR, ALL, or both. GAPDH was used as loading control. E. GSH levels measured in media after conditioning with BV173 ALL cells, 3T3-L1 adipocytes, or both, for 48 hours. * P

    Article Snippet: Cell culture All human ALL cell lines (BV173, RS4;11, and Nalm6) and murine pre-adipocyte 3T3-L1 were from ATCC.

    Techniques: Confocal Microscopy, Fluorescence, Transformation Assay, Expressing, Real-time Polymerase Chain Reaction, Western Blot

    Oxidative stress in adipocytes leads to secretion of survival factors that protect ALL cells from DNR ( A ) Representative western blot of HIF-1α in ChubS7 adipocytes treated with CoCl 2 . GAPDH was used as loading control. ( B ) 3T3-L1 gene expression by qPCR with CoCl 2 treatment for 24 hours ( n = 4). ( C ) Viable cell number of DNR-treated 8093 ALL cells (left) or BV173 cells (right) in the presence of ACM from 3T3-L1 or ChubS7. ACM spiked with CoCl 2 were denoted as (+ CoCl 2 ) and ACM conditioned in the presence of 30 μM CoCl 2 as (w/ CoCl 2 , n = 4–8). * P

    Journal: Oncotarget

    Article Title: Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response

    doi: 10.18632/oncotarget.12246

    Figure Lengend Snippet: Oxidative stress in adipocytes leads to secretion of survival factors that protect ALL cells from DNR ( A ) Representative western blot of HIF-1α in ChubS7 adipocytes treated with CoCl 2 . GAPDH was used as loading control. ( B ) 3T3-L1 gene expression by qPCR with CoCl 2 treatment for 24 hours ( n = 4). ( C ) Viable cell number of DNR-treated 8093 ALL cells (left) or BV173 cells (right) in the presence of ACM from 3T3-L1 or ChubS7. ACM spiked with CoCl 2 were denoted as (+ CoCl 2 ) and ACM conditioned in the presence of 30 μM CoCl 2 as (w/ CoCl 2 , n = 4–8). * P

    Article Snippet: Cell culture All human ALL cell lines (BV173, RS4;11, and Nalm6) and murine pre-adipocyte 3T3-L1 were from ATCC.

    Techniques: Western Blot, Expressing, Real-time Polymerase Chain Reaction

    Exogenous antioxidants protect ALL cells from DNR ( A ) BV173 and Nalm6 treated with DNR or DNR + GSH (20 mM, n = 4). ( B ) BV173 and Nalm6 treated with DNR or DNR + NAC (20 mM, n = 3–4). ( C ) Cell viability and intracellular ROS evaluation using flow cytometry with DAPI and CellROX ® staining of BV173 (top two panels) and Nalm6 (bottom two panels) treated with DNR alone or DNR and NAC n = 5. * P

    Journal: Oncotarget

    Article Title: Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response

    doi: 10.18632/oncotarget.12246

    Figure Lengend Snippet: Exogenous antioxidants protect ALL cells from DNR ( A ) BV173 and Nalm6 treated with DNR or DNR + GSH (20 mM, n = 4). ( B ) BV173 and Nalm6 treated with DNR or DNR + NAC (20 mM, n = 3–4). ( C ) Cell viability and intracellular ROS evaluation using flow cytometry with DAPI and CellROX ® staining of BV173 (top two panels) and Nalm6 (bottom two panels) treated with DNR alone or DNR and NAC n = 5. * P

    Article Snippet: Cell culture All human ALL cell lines (BV173, RS4;11, and Nalm6) and murine pre-adipocyte 3T3-L1 were from ATCC.

    Techniques: Flow Cytometry, Cytometry, Staining

    Adipocytes protect ALL from oxidative stress induced cell death ( A ) ALL cells co-cultured in TransWells over 3T3-L1 and ChubS7 pre-adipocytes (hatched bars) and adipocytes (black bars) with 72 hour DNR treatment (8093 35 nM, BV173 100 nM, RS4;11 100 nM, and Nalm6 200 nM). No feeder condition is where ALL cells were cultured alone ( n = 3–5). ( B ) One representative image of western blot of Caspase 3 (37 kDa) and cleaved caspase 3 (19 and 17 kDa) in BV173 cells treated with DNR for 24 hours in the presence or absence of adipocytes. Images were histogram stretched in a consistent manner to increase brightness for publication. Quantification of the ratio of cleaved (both bands) over total caspase 3 (band at 37 kDa) is shown on the right ( n = 3). ( C ) BV173 ALL cells cultured over 3T3-L1 cells and treated with various doses of doxorubicin (Dox). ( D ) 8093 cells treated with 35 nM DNR in 3T3-L1 ACM and ALCM (left, n = 6); BV173 cells treated with 100 nM DNR in ChubS7 ACM and ALCM (right, n = 5). ( E ) Quantification of cleaved over total caspase 3 of 8093 ALL cells after 24 hours treatment with 25 nM DNR with and without ALCM. ( F ) Annexin V staining of human ALL cells after 24 hour exposure to DNR with or without ALCM. * P

    Journal: Oncotarget

    Article Title: Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response

    doi: 10.18632/oncotarget.12246

    Figure Lengend Snippet: Adipocytes protect ALL from oxidative stress induced cell death ( A ) ALL cells co-cultured in TransWells over 3T3-L1 and ChubS7 pre-adipocytes (hatched bars) and adipocytes (black bars) with 72 hour DNR treatment (8093 35 nM, BV173 100 nM, RS4;11 100 nM, and Nalm6 200 nM). No feeder condition is where ALL cells were cultured alone ( n = 3–5). ( B ) One representative image of western blot of Caspase 3 (37 kDa) and cleaved caspase 3 (19 and 17 kDa) in BV173 cells treated with DNR for 24 hours in the presence or absence of adipocytes. Images were histogram stretched in a consistent manner to increase brightness for publication. Quantification of the ratio of cleaved (both bands) over total caspase 3 (band at 37 kDa) is shown on the right ( n = 3). ( C ) BV173 ALL cells cultured over 3T3-L1 cells and treated with various doses of doxorubicin (Dox). ( D ) 8093 cells treated with 35 nM DNR in 3T3-L1 ACM and ALCM (left, n = 6); BV173 cells treated with 100 nM DNR in ChubS7 ACM and ALCM (right, n = 5). ( E ) Quantification of cleaved over total caspase 3 of 8093 ALL cells after 24 hours treatment with 25 nM DNR with and without ALCM. ( F ) Annexin V staining of human ALL cells after 24 hour exposure to DNR with or without ALCM. * P

    Article Snippet: Cell culture All human ALL cell lines (BV173, RS4;11, and Nalm6) and murine pre-adipocyte 3T3-L1 were from ATCC.

    Techniques: Cell Culture, Western Blot, Staining

    Co-localization and Physical Interactions of Native Ikaros and BTK Proteins in Human Cells. [A] Nuclear co-localization of Native IK and BTK. ALL-N1 cells were fixed and stained with polyclonal rabbit anti-IK1 (primary Ab)/Alexa Fluor 568 F(ab') 2 fragment of goat anti-rabbit IgG (secondary Ab) (red) and mouse anti-BTK MoAb (primary Ab)/Alexa Fluor 488 goat anti-mouse IgG (secondary Ab) (green) antibodies. Nuclei were stained with blue fluorescent dye 4′,6-diamidino-2-phenylindole (DAPI). MERGE panels depict the merge three-color confocal image showing co-localization of IK1 and BTK in DAPI-stained nucleus as magenta immunofluorescent foci (System magnification: 315×). Representative foci of colocalization are indicated with white arrowheads. [B] Co-immunoprecipitation of Native IK and BTK. B1 depicts the results of the BTK Western blot analysis of the IK and BTK immune complexes immunoprecipitated (IP) from ALL-N1 cells. B.2 depicts the results of the IK Western blot analysis of the BTK and IK immune complexes from the same cells. Controls included immunoprecipitations performed without using a primary (1 0 ) antibody.

    Journal: PLoS ONE

    Article Title: Regulatory Phosphorylation of Ikaros by Bruton's Tyrosine Kinase

    doi: 10.1371/journal.pone.0071302

    Figure Lengend Snippet: Co-localization and Physical Interactions of Native Ikaros and BTK Proteins in Human Cells. [A] Nuclear co-localization of Native IK and BTK. ALL-N1 cells were fixed and stained with polyclonal rabbit anti-IK1 (primary Ab)/Alexa Fluor 568 F(ab') 2 fragment of goat anti-rabbit IgG (secondary Ab) (red) and mouse anti-BTK MoAb (primary Ab)/Alexa Fluor 488 goat anti-mouse IgG (secondary Ab) (green) antibodies. Nuclei were stained with blue fluorescent dye 4′,6-diamidino-2-phenylindole (DAPI). MERGE panels depict the merge three-color confocal image showing co-localization of IK1 and BTK in DAPI-stained nucleus as magenta immunofluorescent foci (System magnification: 315×). Representative foci of colocalization are indicated with white arrowheads. [B] Co-immunoprecipitation of Native IK and BTK. B1 depicts the results of the BTK Western blot analysis of the IK and BTK immune complexes immunoprecipitated (IP) from ALL-N1 cells. B.2 depicts the results of the IK Western blot analysis of the BTK and IK immune complexes from the same cells. Controls included immunoprecipitations performed without using a primary (1 0 ) antibody.

    Article Snippet: We also used the human cell lines ALL-N1 (B-precursor ALL xenograft cell line), RAJI (Burkitt's leukemia/lymphoma; ATCC®, CCL-86) and DAUDI (Burkitt's leukemia/lymphoma; ATCC®, CCL-213).

    Techniques: Staining, Immunoprecipitation, Western Blot

    The expression of HO-1 is strongly correlated with IK6 A. Differential expression of HO-1 mRNA in adult BCR-ABL1-positive B-ALL patients and normal CD34 + cells were determined by qRT-PCR. B. Western blot analysis of Ikaros expression in IK6-positive and –negative patients. C, D. Western blot analysis of HO-1 expression at protein level in adult BCR-ABL1-positive B-ALL patients and normal CD34 + cells. E. Scatterplot representation of the correlation between the expression of HO-1 and Ikaros in patient samples. F. Co-immunoprecipitation assay to verify the interaction of Flag-IK6 with Myc-HO-1 in SupB15 cells (upper panel) and the endogenous interaction of Ikaros with HO-1 in primary leukemic cells (lower panel). (Pts=patients).

    Journal: Oncotarget

    Article Title: Targeting of heme oxygenase-1 attenuates the negative impact of Ikaros isoform 6 in adult BCR-ABL1-positive B-ALL

    doi: 10.18632/oncotarget.10725

    Figure Lengend Snippet: The expression of HO-1 is strongly correlated with IK6 A. Differential expression of HO-1 mRNA in adult BCR-ABL1-positive B-ALL patients and normal CD34 + cells were determined by qRT-PCR. B. Western blot analysis of Ikaros expression in IK6-positive and –negative patients. C, D. Western blot analysis of HO-1 expression at protein level in adult BCR-ABL1-positive B-ALL patients and normal CD34 + cells. E. Scatterplot representation of the correlation between the expression of HO-1 and Ikaros in patient samples. F. Co-immunoprecipitation assay to verify the interaction of Flag-IK6 with Myc-HO-1 in SupB15 cells (upper panel) and the endogenous interaction of Ikaros with HO-1 in primary leukemic cells (lower panel). (Pts=patients).

    Article Snippet: Cell culture Human BCR-ABL1-positive B-ALL cell lines SupB15 was purchased from the American Type Culture Collection (Manassas, VA).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Co-Immunoprecipitation Assay

    IK6 is highly expressed in adult BCR-ABL1-positive B-ALL patients A. Schematic diagram of the full-length IKZF1 cDNA and the different isoforms detected in our samples. F: N-terminal zinc-fingers show DNA-binding activity, and C-terminal zinc fingers mediate dimerization of the protein. Ex indicates exon. B. Expressions of the different IKZF1 isoforms in 42 BCR-ABL1-positive B-ALLsamples were determined by RT-PCR. IK1(945bp), IK2(884bp), IK4 (458bp), IK6(255bp). C. Sequencing analysis of IK6 isoform in which exon 3 is juxtaposed with exon8. D. Kaplan-meier estimation of DFS in IK6-positive and -negative group. E. Cumulative incidence of relapse curves by IKZF1 status in our samples, with 3-year estimates. CR1, first complete remission.

    Journal: Oncotarget

    Article Title: Targeting of heme oxygenase-1 attenuates the negative impact of Ikaros isoform 6 in adult BCR-ABL1-positive B-ALL

    doi: 10.18632/oncotarget.10725

    Figure Lengend Snippet: IK6 is highly expressed in adult BCR-ABL1-positive B-ALL patients A. Schematic diagram of the full-length IKZF1 cDNA and the different isoforms detected in our samples. F: N-terminal zinc-fingers show DNA-binding activity, and C-terminal zinc fingers mediate dimerization of the protein. Ex indicates exon. B. Expressions of the different IKZF1 isoforms in 42 BCR-ABL1-positive B-ALLsamples were determined by RT-PCR. IK1(945bp), IK2(884bp), IK4 (458bp), IK6(255bp). C. Sequencing analysis of IK6 isoform in which exon 3 is juxtaposed with exon8. D. Kaplan-meier estimation of DFS in IK6-positive and -negative group. E. Cumulative incidence of relapse curves by IKZF1 status in our samples, with 3-year estimates. CR1, first complete remission.

    Article Snippet: Cell culture Human BCR-ABL1-positive B-ALL cell lines SupB15 was purchased from the American Type Culture Collection (Manassas, VA).

    Techniques: Zinc-Fingers, Binding Assay, Activity Assay, Reverse Transcription Polymerase Chain Reaction, Sequencing