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human a427 cell line  (ATCC)


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    Structured Review

    ATCC human a427 cell line
    ( A ) Percentage of proliferation inhibition of A549, <t>A427</t> and H460 cell lines treated with increasing doses of XMD8-92 or Seliciclib or in combination (top) 48 h after treatment and representative crystal violet-stained cells 72 h after drug treatment (bottom). The combination index (CI) showing the synergistic effect of combination of the 2 drugs is indicated; n = 3. ( B – D ) Relative quantification of Annexin V (AV) + Annexin V/PI (AV/PI)-positive cells by flow cytometry; n = 4 ( B ), colony forming capacity; n = 3 ( C ) and percentage of cell migration; n = 10 ( D ) of A549 cells treated with 10 µM XMD8-92 or Seliciclib or in combination, except for the colony formation assay in which cells were treated with 5 µM of each drug. ( E ) Immunoblot analysis of the indicated targets in A549 cells treated with the indicated doses of Seliciclib or XMD8-92 or in combination for 24 h. ( F ) Immunoblot analysis of the indicated targets in A549 cells treated with 10 µM XMD8-92 or 10 µM Seliciclib or in combination for 24 h. ( G ) Immunoblot analysis for the indicated targets in A549 cells transduced with shRNA control (pLKO.1 hygro + Tet-pLKO-puro) or a shRNA against CDK5 (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro), or a shRNA against ERK5 (pLKO.1 hygro-shERK5 + Tet-pLKO-puro) or in combination (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro-shERK5). After transduction and selection, cells were harvested for protein extraction 72 h after doxycycline (1 μg/mL) induction. ( H , I ) Relative cell number ( H ) and Annexin V (AV) + Annexin V/PI (AV/PI)-positive cell quantification by flow cytometry ( I ) in A549 cells treated as in ( G ) 72 h after doxycycline (1 μg/mL) induction; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples. .
    Human A427 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 378 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+a427+cell+line/pmc11473843-4-0-14?v=ATCC
    Average 96 stars, based on 378 article reviews
    human a427 cell line - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer"

    Article Title: ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer

    Journal: EMBO Molecular Medicine

    doi: 10.1038/s44321-024-00138-7

    ( A ) Percentage of proliferation inhibition of A549, A427 and H460 cell lines treated with increasing doses of XMD8-92 or Seliciclib or in combination (top) 48 h after treatment and representative crystal violet-stained cells 72 h after drug treatment (bottom). The combination index (CI) showing the synergistic effect of combination of the 2 drugs is indicated; n = 3. ( B – D ) Relative quantification of Annexin V (AV) + Annexin V/PI (AV/PI)-positive cells by flow cytometry; n = 4 ( B ), colony forming capacity; n = 3 ( C ) and percentage of cell migration; n = 10 ( D ) of A549 cells treated with 10 µM XMD8-92 or Seliciclib or in combination, except for the colony formation assay in which cells were treated with 5 µM of each drug. ( E ) Immunoblot analysis of the indicated targets in A549 cells treated with the indicated doses of Seliciclib or XMD8-92 or in combination for 24 h. ( F ) Immunoblot analysis of the indicated targets in A549 cells treated with 10 µM XMD8-92 or 10 µM Seliciclib or in combination for 24 h. ( G ) Immunoblot analysis for the indicated targets in A549 cells transduced with shRNA control (pLKO.1 hygro + Tet-pLKO-puro) or a shRNA against CDK5 (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro), or a shRNA against ERK5 (pLKO.1 hygro-shERK5 + Tet-pLKO-puro) or in combination (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro-shERK5). After transduction and selection, cells were harvested for protein extraction 72 h after doxycycline (1 μg/mL) induction. ( H , I ) Relative cell number ( H ) and Annexin V (AV) + Annexin V/PI (AV/PI)-positive cell quantification by flow cytometry ( I ) in A549 cells treated as in ( G ) 72 h after doxycycline (1 μg/mL) induction; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples. .
    Figure Legend Snippet: ( A ) Percentage of proliferation inhibition of A549, A427 and H460 cell lines treated with increasing doses of XMD8-92 or Seliciclib or in combination (top) 48 h after treatment and representative crystal violet-stained cells 72 h after drug treatment (bottom). The combination index (CI) showing the synergistic effect of combination of the 2 drugs is indicated; n = 3. ( B – D ) Relative quantification of Annexin V (AV) + Annexin V/PI (AV/PI)-positive cells by flow cytometry; n = 4 ( B ), colony forming capacity; n = 3 ( C ) and percentage of cell migration; n = 10 ( D ) of A549 cells treated with 10 µM XMD8-92 or Seliciclib or in combination, except for the colony formation assay in which cells were treated with 5 µM of each drug. ( E ) Immunoblot analysis of the indicated targets in A549 cells treated with the indicated doses of Seliciclib or XMD8-92 or in combination for 24 h. ( F ) Immunoblot analysis of the indicated targets in A549 cells treated with 10 µM XMD8-92 or 10 µM Seliciclib or in combination for 24 h. ( G ) Immunoblot analysis for the indicated targets in A549 cells transduced with shRNA control (pLKO.1 hygro + Tet-pLKO-puro) or a shRNA against CDK5 (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro), or a shRNA against ERK5 (pLKO.1 hygro-shERK5 + Tet-pLKO-puro) or in combination (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro-shERK5). After transduction and selection, cells were harvested for protein extraction 72 h after doxycycline (1 μg/mL) induction. ( H , I ) Relative cell number ( H ) and Annexin V (AV) + Annexin V/PI (AV/PI)-positive cell quantification by flow cytometry ( I ) in A549 cells treated as in ( G ) 72 h after doxycycline (1 μg/mL) induction; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples. .

    Techniques Used: Inhibition, Staining, Quantitative Proteomics, Flow Cytometry, Migration, Colony Assay, Western Blot, Transduction, shRNA, Control, Selection, Protein Extraction

    Relative quantification of cell death by flow cytometry analysis of Annexin V-Atto 633 (AV) + Annexin V/PI (AV/PI)-positive (left) and colony number (right) of A427 cells treated with XMD8-92 or Seliciclib (10 µM for apoptosis assay and 2.5 µM for colony formation each, respectively) alone or in combination; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples.
    Figure Legend Snippet: Relative quantification of cell death by flow cytometry analysis of Annexin V-Atto 633 (AV) + Annexin V/PI (AV/PI)-positive (left) and colony number (right) of A427 cells treated with XMD8-92 or Seliciclib (10 µM for apoptosis assay and 2.5 µM for colony formation each, respectively) alone or in combination; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples.

    Techniques Used: Quantitative Proteomics, Flow Cytometry, Apoptosis Assay

    Reagents and tools table
    Figure Legend Snippet: Reagents and tools table

    Techniques Used: Recombinant, Plasmid Preparation, Sequencing, shRNA, Reverse Transcription Polymerase Chain Reaction, Transfection, Western Blot, In Vitro, In Vivo, cDNA Synthesis, TUNEL Assay, Software



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    ( A ) Percentage of proliferation inhibition of A549, <t>A427</t> and H460 cell lines treated with increasing doses of XMD8-92 or Seliciclib or in combination (top) 48 h after treatment and representative crystal violet-stained cells 72 h after drug treatment (bottom). The combination index (CI) showing the synergistic effect of combination of the 2 drugs is indicated; n = 3. ( B – D ) Relative quantification of Annexin V (AV) + Annexin V/PI (AV/PI)-positive cells by flow cytometry; n = 4 ( B ), colony forming capacity; n = 3 ( C ) and percentage of cell migration; n = 10 ( D ) of A549 cells treated with 10 µM XMD8-92 or Seliciclib or in combination, except for the colony formation assay in which cells were treated with 5 µM of each drug. ( E ) Immunoblot analysis of the indicated targets in A549 cells treated with the indicated doses of Seliciclib or XMD8-92 or in combination for 24 h. ( F ) Immunoblot analysis of the indicated targets in A549 cells treated with 10 µM XMD8-92 or 10 µM Seliciclib or in combination for 24 h. ( G ) Immunoblot analysis for the indicated targets in A549 cells transduced with shRNA control (pLKO.1 hygro + Tet-pLKO-puro) or a shRNA against CDK5 (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro), or a shRNA against ERK5 (pLKO.1 hygro-shERK5 + Tet-pLKO-puro) or in combination (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro-shERK5). After transduction and selection, cells were harvested for protein extraction 72 h after doxycycline (1 μg/mL) induction. ( H , I ) Relative cell number ( H ) and Annexin V (AV) + Annexin V/PI (AV/PI)-positive cell quantification by flow cytometry ( I ) in A549 cells treated as in ( G ) 72 h after doxycycline (1 μg/mL) induction; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples. .
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    cEMSY expression level correlates with an enhanced immunotherapy response. A, Illustrative images of 65 lung <t>adenocarcinoma</t> (LUAD) tissues showing cEMSY (magenta), CD8 + T cells (green), CD11c + DCs (white), and DAPI (blue). Samples were categorized based on cEMSY fluorescence into cEMSY high (above the mean intensity) and cEMSY low (below the mean intensity). B, Analysis of the proportion of intratumor CD11c + DCs and CD8 + T cells within DAPI + cells across the two cEMSY stratifications. Data presented as median ± quartiles for groups cEMSY low ( n = 37) and cEMSY high ( n = 28). C, The Kaplan–Meier curve for the disease-free survival (DFS) of patients with LUAD, who were divided into two groups according to the mean expression of cEMSY. D, Heatmap showing Spearman correlations between CD11c + DCs and CD8 + T-cell infiltration and cEMSY signature gene set variation analysis score of indicated gene sets in each TCGA cohort. ACC, adrenocortical carcinoma; BLCA, bladder urothelial Carcinoma; BRCA, breast invasive carcinoma; CESC, cervical squamous cell carcinoma and endocervical adenocarcinoma; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LGG, lower grade glioma; LIHC, liver hepatocellular carcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; TGCT, tescticular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma. E, cEMSY signature expression level of the responders (R) and nonresponders (NR) of two representative LUAD ICB cohorts. F, Progression-free survival (PFS) of ICB cohorts based on the level of cEMSY signature. Statistics were applied using Spearman rank correlation, Student t test, or log-rank test.
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    Figure 4. Inhibition of tumor cell growth by (a) stachybotrydial acetate and (b) acetoxystachybotrydial acetate. MCF7 NucLight Green cells, A431 cells and <t>A427</t> cells were treated with 1 µM (□) and 100 µM (∆) of stachybotrydial acetate or acetoxystachybotrydial acetate or 1% DMSO as control (•) for 48 h. Cell confluence was monitored over 48 h using IncuCyte® S3 live cell imaging system and analyzed using the IncuCyte® S3 2017A software.
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    Figure 4. Inhibition of tumor cell growth by (a) stachybotrydial acetate and (b) acetoxystachybotrydial acetate. MCF7 NucLight Green cells, A431 cells and <t>A427</t> cells were treated with 1 µM (□) and 100 µM (∆) of stachybotrydial acetate or acetoxystachybotrydial acetate or 1% DMSO as control (•) for 48 h. Cell confluence was monitored over 48 h using IncuCyte® S3 live cell imaging system and analyzed using the IncuCyte® S3 2017A software.
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    Figure 4. Inhibition of tumor cell growth by (a) stachybotrydial acetate and (b) acetoxystachybotrydial acetate. MCF7 NucLight Green cells, A431 cells and <t>A427</t> cells were treated with 1 µM (□) and 100 µM (∆) of stachybotrydial acetate or acetoxystachybotrydial acetate or 1% DMSO as control (•) for 48 h. Cell confluence was monitored over 48 h using IncuCyte® S3 live cell imaging system and analyzed using the IncuCyte® S3 2017A software.
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    Image Search Results


    ( A ) Percentage of proliferation inhibition of A549, A427 and H460 cell lines treated with increasing doses of XMD8-92 or Seliciclib or in combination (top) 48 h after treatment and representative crystal violet-stained cells 72 h after drug treatment (bottom). The combination index (CI) showing the synergistic effect of combination of the 2 drugs is indicated; n = 3. ( B – D ) Relative quantification of Annexin V (AV) + Annexin V/PI (AV/PI)-positive cells by flow cytometry; n = 4 ( B ), colony forming capacity; n = 3 ( C ) and percentage of cell migration; n = 10 ( D ) of A549 cells treated with 10 µM XMD8-92 or Seliciclib or in combination, except for the colony formation assay in which cells were treated with 5 µM of each drug. ( E ) Immunoblot analysis of the indicated targets in A549 cells treated with the indicated doses of Seliciclib or XMD8-92 or in combination for 24 h. ( F ) Immunoblot analysis of the indicated targets in A549 cells treated with 10 µM XMD8-92 or 10 µM Seliciclib or in combination for 24 h. ( G ) Immunoblot analysis for the indicated targets in A549 cells transduced with shRNA control (pLKO.1 hygro + Tet-pLKO-puro) or a shRNA against CDK5 (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro), or a shRNA against ERK5 (pLKO.1 hygro-shERK5 + Tet-pLKO-puro) or in combination (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro-shERK5). After transduction and selection, cells were harvested for protein extraction 72 h after doxycycline (1 μg/mL) induction. ( H , I ) Relative cell number ( H ) and Annexin V (AV) + Annexin V/PI (AV/PI)-positive cell quantification by flow cytometry ( I ) in A549 cells treated as in ( G ) 72 h after doxycycline (1 μg/mL) induction; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples. .

    Journal: EMBO Molecular Medicine

    Article Title: ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer

    doi: 10.1038/s44321-024-00138-7

    Figure Lengend Snippet: ( A ) Percentage of proliferation inhibition of A549, A427 and H460 cell lines treated with increasing doses of XMD8-92 or Seliciclib or in combination (top) 48 h after treatment and representative crystal violet-stained cells 72 h after drug treatment (bottom). The combination index (CI) showing the synergistic effect of combination of the 2 drugs is indicated; n = 3. ( B – D ) Relative quantification of Annexin V (AV) + Annexin V/PI (AV/PI)-positive cells by flow cytometry; n = 4 ( B ), colony forming capacity; n = 3 ( C ) and percentage of cell migration; n = 10 ( D ) of A549 cells treated with 10 µM XMD8-92 or Seliciclib or in combination, except for the colony formation assay in which cells were treated with 5 µM of each drug. ( E ) Immunoblot analysis of the indicated targets in A549 cells treated with the indicated doses of Seliciclib or XMD8-92 or in combination for 24 h. ( F ) Immunoblot analysis of the indicated targets in A549 cells treated with 10 µM XMD8-92 or 10 µM Seliciclib or in combination for 24 h. ( G ) Immunoblot analysis for the indicated targets in A549 cells transduced with shRNA control (pLKO.1 hygro + Tet-pLKO-puro) or a shRNA against CDK5 (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro), or a shRNA against ERK5 (pLKO.1 hygro-shERK5 + Tet-pLKO-puro) or in combination (Tet-pLKO-puro-shCDK5 + pLKO.1 hygro-shERK5). After transduction and selection, cells were harvested for protein extraction 72 h after doxycycline (1 μg/mL) induction. ( H , I ) Relative cell number ( H ) and Annexin V (AV) + Annexin V/PI (AV/PI)-positive cell quantification by flow cytometry ( I ) in A549 cells treated as in ( G ) 72 h after doxycycline (1 μg/mL) induction; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples. .

    Article Snippet: Human: A427 cell line , Prof. John Minna (UTSW Medical Center, Dallas, USA) , ATCC # HTB-53.

    Techniques: Inhibition, Staining, Quantitative Proteomics, Flow Cytometry, Migration, Colony Assay, Western Blot, Transduction, shRNA, Control, Selection, Protein Extraction

    Relative quantification of cell death by flow cytometry analysis of Annexin V-Atto 633 (AV) + Annexin V/PI (AV/PI)-positive (left) and colony number (right) of A427 cells treated with XMD8-92 or Seliciclib (10 µM for apoptosis assay and 2.5 µM for colony formation each, respectively) alone or in combination; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples.

    Journal: EMBO Molecular Medicine

    Article Title: ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer

    doi: 10.1038/s44321-024-00138-7

    Figure Lengend Snippet: Relative quantification of cell death by flow cytometry analysis of Annexin V-Atto 633 (AV) + Annexin V/PI (AV/PI)-positive (left) and colony number (right) of A427 cells treated with XMD8-92 or Seliciclib (10 µM for apoptosis assay and 2.5 µM for colony formation each, respectively) alone or in combination; n = 3. Graphical data are mean ± SD. Statistical analyses were done using one-way ANOVA; n , number of biologically independent samples.

    Article Snippet: Human: A427 cell line , Prof. John Minna (UTSW Medical Center, Dallas, USA) , ATCC # HTB-53.

    Techniques: Quantitative Proteomics, Flow Cytometry, Apoptosis Assay

    Reagents and tools table

    Journal: EMBO Molecular Medicine

    Article Title: ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer

    doi: 10.1038/s44321-024-00138-7

    Figure Lengend Snippet: Reagents and tools table

    Article Snippet: Human: A427 cell line , Prof. John Minna (UTSW Medical Center, Dallas, USA) , ATCC # HTB-53.

    Techniques: Recombinant, Plasmid Preparation, Sequencing, shRNA, Reverse Transcription Polymerase Chain Reaction, Transfection, Western Blot, In Vitro, In Vivo, cDNA Synthesis, TUNEL Assay, Software

    cEMSY expression level correlates with an enhanced immunotherapy response. A, Illustrative images of 65 lung adenocarcinoma (LUAD) tissues showing cEMSY (magenta), CD8 + T cells (green), CD11c + DCs (white), and DAPI (blue). Samples were categorized based on cEMSY fluorescence into cEMSY high (above the mean intensity) and cEMSY low (below the mean intensity). B, Analysis of the proportion of intratumor CD11c + DCs and CD8 + T cells within DAPI + cells across the two cEMSY stratifications. Data presented as median ± quartiles for groups cEMSY low ( n = 37) and cEMSY high ( n = 28). C, The Kaplan–Meier curve for the disease-free survival (DFS) of patients with LUAD, who were divided into two groups according to the mean expression of cEMSY. D, Heatmap showing Spearman correlations between CD11c + DCs and CD8 + T-cell infiltration and cEMSY signature gene set variation analysis score of indicated gene sets in each TCGA cohort. ACC, adrenocortical carcinoma; BLCA, bladder urothelial Carcinoma; BRCA, breast invasive carcinoma; CESC, cervical squamous cell carcinoma and endocervical adenocarcinoma; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LGG, lower grade glioma; LIHC, liver hepatocellular carcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; TGCT, tescticular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma. E, cEMSY signature expression level of the responders (R) and nonresponders (NR) of two representative LUAD ICB cohorts. F, Progression-free survival (PFS) of ICB cohorts based on the level of cEMSY signature. Statistics were applied using Spearman rank correlation, Student t test, or log-rank test.

    Journal: Cancer Research

    Article Title: The circRNA cEMSY Induces Immunogenic Cell Death and Boosts Immunotherapy Efficacy in Lung Adenocarcinoma

    doi: 10.1158/0008-5472.CAN-24-1484

    Figure Lengend Snippet: cEMSY expression level correlates with an enhanced immunotherapy response. A, Illustrative images of 65 lung adenocarcinoma (LUAD) tissues showing cEMSY (magenta), CD8 + T cells (green), CD11c + DCs (white), and DAPI (blue). Samples were categorized based on cEMSY fluorescence into cEMSY high (above the mean intensity) and cEMSY low (below the mean intensity). B, Analysis of the proportion of intratumor CD11c + DCs and CD8 + T cells within DAPI + cells across the two cEMSY stratifications. Data presented as median ± quartiles for groups cEMSY low ( n = 37) and cEMSY high ( n = 28). C, The Kaplan–Meier curve for the disease-free survival (DFS) of patients with LUAD, who were divided into two groups according to the mean expression of cEMSY. D, Heatmap showing Spearman correlations between CD11c + DCs and CD8 + T-cell infiltration and cEMSY signature gene set variation analysis score of indicated gene sets in each TCGA cohort. ACC, adrenocortical carcinoma; BLCA, bladder urothelial Carcinoma; BRCA, breast invasive carcinoma; CESC, cervical squamous cell carcinoma and endocervical adenocarcinoma; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LGG, lower grade glioma; LIHC, liver hepatocellular carcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; TGCT, tescticular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma. E, cEMSY signature expression level of the responders (R) and nonresponders (NR) of two representative LUAD ICB cohorts. F, Progression-free survival (PFS) of ICB cohorts based on the level of cEMSY signature. Statistics were applied using Spearman rank correlation, Student t test, or log-rank test.

    Article Snippet: Human bronchial epithelial (HBE) cells and human lung adenocarcinoma cell lines (H358, A549, H23, H1975, PC9, A427, and H373), as well as murine lung adenocarcinoma cell lines (LLC1 and LA795), were obtained from the China Center for Type Culture Collection.

    Techniques: Expressing, Fluorescence

    Figure 4. Inhibition of tumor cell growth by (a) stachybotrydial acetate and (b) acetoxystachybotrydial acetate. MCF7 NucLight Green cells, A431 cells and A427 cells were treated with 1 µM (□) and 100 µM (∆) of stachybotrydial acetate or acetoxystachybotrydial acetate or 1% DMSO as control (•) for 48 h. Cell confluence was monitored over 48 h using IncuCyte® S3 live cell imaging system and analyzed using the IncuCyte® S3 2017A software.

    Journal: Molecules

    Article Title: Natural Compounds Isolated from Stachybotrys chartarum Are Potent Inhibitors of Human Protein Kinase CK2

    doi: 10.3390/molecules26154453

    Figure Lengend Snippet: Figure 4. Inhibition of tumor cell growth by (a) stachybotrydial acetate and (b) acetoxystachybotrydial acetate. MCF7 NucLight Green cells, A431 cells and A427 cells were treated with 1 µM (□) and 100 µM (∆) of stachybotrydial acetate or acetoxystachybotrydial acetate or 1% DMSO as control (•) for 48 h. Cell confluence was monitored over 48 h using IncuCyte® S3 live cell imaging system and analyzed using the IncuCyte® S3 2017A software.

    Article Snippet: For cultivation of A427 human lung carcinoma cell line (purchased from German Collection of Microorganisms and Cell Cultures (DSMZ), No. ACC234, Braunschweig, Germany), Roswell Park Memorial Institute, medium (RPMI1640) supplemented with 2 mM L-glutamine and 10% FCS was used.

    Techniques: Inhibition, Control, Live Cell Imaging, Software

    Figure 5. Phase contrast images of (a) MCF7 cells, (b) A427 cells and (c) A431 cells treated with acetoxystachybotrydial acetate in a concentration of 1 µM and 1% DMSO as control at 0 h, 24 h and 48 h after treatment. Images were taken at tenfold magnification on IncuCyte® live cell imager.

    Journal: Molecules

    Article Title: Natural Compounds Isolated from Stachybotrys chartarum Are Potent Inhibitors of Human Protein Kinase CK2

    doi: 10.3390/molecules26154453

    Figure Lengend Snippet: Figure 5. Phase contrast images of (a) MCF7 cells, (b) A427 cells and (c) A431 cells treated with acetoxystachybotrydial acetate in a concentration of 1 µM and 1% DMSO as control at 0 h, 24 h and 48 h after treatment. Images were taken at tenfold magnification on IncuCyte® live cell imager.

    Article Snippet: For cultivation of A427 human lung carcinoma cell line (purchased from German Collection of Microorganisms and Cell Cultures (DSMZ), No. ACC234, Braunschweig, Germany), Roswell Park Memorial Institute, medium (RPMI1640) supplemented with 2 mM L-glutamine and 10% FCS was used.

    Techniques: Concentration Assay, Control