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ATCC human breast cancer cell lines mda mb 231

Ptch1 is expressed in breast cancer cell lines. A. PTCH1 mRNA expression (log 2 transformed) in various luminal and HER2 breast cancer cell lines (dark green) and in TNBC cell lines (other colors). TNBC cell lines are depicted according to the “Lehmann TNBC subtype” nomenclature : basal-like 1 (yellow), basal-like 2 (pale green), immunomodulatory (brown), luminal androgen receptor (dark pink), mesenchymal (pale pink) and mesenchymal stem-like (pink). B. PTCH1 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from TNBC cell lines <t>(MDA-MB-231,</t> HCC-38 and MDA-MB-468) with antibodies directed against PTCH1. PTCH1 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*).

Human Breast Cancer Cell Lines Mda Mb 231, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 5641 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers"

Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

Journal: Translational Oncology

doi: 10.1016/j.tranon.2026.102777

Figure Legend Snippet: Ptch1 is expressed in breast cancer cell lines. A. PTCH1 mRNA expression (log 2 transformed) in various luminal and HER2 breast cancer cell lines (dark green) and in TNBC cell lines (other colors). TNBC cell lines are depicted according to the “Lehmann TNBC subtype” nomenclature : basal-like 1 (yellow), basal-like 2 (pale green), immunomodulatory (brown), luminal androgen receptor (dark pink), mesenchymal (pale pink) and mesenchymal stem-like (pink). B. PTCH1 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from TNBC cell lines (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against PTCH1. PTCH1 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*).

Techniques Used: Expressing, Transformation Assay, Western Blot, Software

PTCH1 drug efflux inhibitor PAH increases the sensitivity of TNBC cells to chemotherapy . Cell viability was measured after 24 h or 48 h treatment with increasing concentration of docetaxel or doxorubicin respectively on MDA-MB-231, MDA-MB-468 and HCC-38 cell lines in the absence or the presence of 15µM PAH. IC 50 values (corresponding to the concentration of chemotherapy inducing 50% of cell death) were calculated. Data reported are the mean ± SEM of at least 3 independent experiments. Significance is attained at P < 0.05 (*).

Figure Legend Snippet: PTCH1 drug efflux inhibitor PAH increases the sensitivity of TNBC cells to chemotherapy . Cell viability was measured after 24 h or 48 h treatment with increasing concentration of docetaxel or doxorubicin respectively on MDA-MB-231, MDA-MB-468 and HCC-38 cell lines in the absence or the presence of 15µM PAH. IC 50 values (corresponding to the concentration of chemotherapy inducing 50% of cell death) were calculated. Data reported are the mean ± SEM of at least 3 independent experiments. Significance is attained at P < 0.05 (*).

Techniques Used: Concentration Assay

Other multidrug transporters are expressed in TNBC cell lines. A. P-gp and ABCG2 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from each TNBC cell line (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against P-gp or ABCG2 and GAPDH. B. P-gp, ABCG2 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*). ** P < 0.01; *** P < 0.001; ns P > 0.05.

Figure Legend Snippet: Other multidrug transporters are expressed in TNBC cell lines. A. P-gp and ABCG2 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from each TNBC cell line (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against P-gp or ABCG2 and GAPDH. B. P-gp, ABCG2 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*). ** P < 0.01; *** P < 0.001; ns P > 0.05.

Techniques Used: Expressing, Western Blot, Software

PAH increases docetaxel efficacy against TNBC spheroids. MDA-MB-231 cells were plated in ultra-low attachment surface 24 well plates in complete medium and treated with increasing concentrations of docetaxel in the presence of DMSO (control, 0 PAH), PAH 10 µM or 30 µM. After 2 weeks pictures were taken using Cytation 5 cell imaging system from Biotek. The surface of spheroids was calculated and reported after normalization on the condition without docetaxel for each concentration of PAH.

Figure Legend Snippet: PAH increases docetaxel efficacy against TNBC spheroids. MDA-MB-231 cells were plated in ultra-low attachment surface 24 well plates in complete medium and treated with increasing concentrations of docetaxel in the presence of DMSO (control, 0 PAH), PAH 10 µM or 30 µM. After 2 weeks pictures were taken using Cytation 5 cell imaging system from Biotek. The surface of spheroids was calculated and reported after normalization on the condition without docetaxel for each concentration of PAH.

Techniques Used: Control, Imaging, Concentration Assay

PAH addition to chemotherapy inhibits migration of TNBC cells. A. 100000 cells were seeded on membrane from Transwell plates. Cells were treated 24 h with doxorubicin ± 15µM PAH or 48 h with docetaxel ± 15µM PAH. After fixation and staining with crystal violet, wells were observed on a microscope with X5 objective. B. Migration was measured using a wound-healing assay. A wound was performed on MDA-MB-231 confluent cells seeded in 24 well plates. The medium was replaced by fresh medium containing 5 µM docetaxel in the absence of PAH, or the presence of 5 µM PAH. Two pictures were taken at two different points of each well immediately after wound, and 3 days after wound with 5X objective. The width of the wound was measured using ImageJ software and reported as final wound width/initial wound width in percentage. Data presented are the mean ± SEM of 3 independent experiments. Significance is attained at P < 0.05.

Figure Legend Snippet: PAH addition to chemotherapy inhibits migration of TNBC cells. A. 100000 cells were seeded on membrane from Transwell plates. Cells were treated 24 h with doxorubicin ± 15µM PAH or 48 h with docetaxel ± 15µM PAH. After fixation and staining with crystal violet, wells were observed on a microscope with X5 objective. B. Migration was measured using a wound-healing assay. A wound was performed on MDA-MB-231 confluent cells seeded in 24 well plates. The medium was replaced by fresh medium containing 5 µM docetaxel in the absence of PAH, or the presence of 5 µM PAH. Two pictures were taken at two different points of each well immediately after wound, and 3 days after wound with 5X objective. The width of the wound was measured using ImageJ software and reported as final wound width/initial wound width in percentage. Data presented are the mean ± SEM of 3 independent experiments. Significance is attained at P < 0.05.

Techniques Used: Migration, Membrane, Staining, Microscopy, Wound Healing Assay, Software

PTCH1 contributes to the efflux of doxorubicin from TNBC cells. A. PTCH1 protein expression (left panel) and intracellular doxorubicin (right panel) were analyzed 16 h after transfection of MDA-MB-231 cells with PTCH1-siRNA or negative-control-siRNA. PTCH1 and GAPDH western blot signals were quantified using ImageJ software (left panel). For doxorubicin accumulation measurements (right panel), MDA-MB-231 cells were grown on slides and transfected with PTCH1-siRNA or negative-control-siRNA. After incubation with 10 µM doxorubicin, 3 coverslips were fixed for doxorubicin loading control; the other coverslips were incubated with efflux buffer and fixed. B. Docetaxel inhibits the accumulation of doxorubicin in MDA-MB-231 cells. Cells on coverslip were incubated with 10 µM doxorubicin or 10 µM doxorubicin and 50 µM docetaxel. Doxorubicin fluorescence images were acquired by epifluorescence microscopy using a 40X objective, and doxorubicin fluorescence was quantified using ImageJ software for about 100 cells per condition per experiment. Histograms are the mean ± SEM of 3 independent experiments. Significance is attained at P < 0.05.

Figure Legend Snippet: PTCH1 contributes to the efflux of doxorubicin from TNBC cells. A. PTCH1 protein expression (left panel) and intracellular doxorubicin (right panel) were analyzed 16 h after transfection of MDA-MB-231 cells with PTCH1-siRNA or negative-control-siRNA. PTCH1 and GAPDH western blot signals were quantified using ImageJ software (left panel). For doxorubicin accumulation measurements (right panel), MDA-MB-231 cells were grown on slides and transfected with PTCH1-siRNA or negative-control-siRNA. After incubation with 10 µM doxorubicin, 3 coverslips were fixed for doxorubicin loading control; the other coverslips were incubated with efflux buffer and fixed. B. Docetaxel inhibits the accumulation of doxorubicin in MDA-MB-231 cells. Cells on coverslip were incubated with 10 µM doxorubicin or 10 µM doxorubicin and 50 µM docetaxel. Doxorubicin fluorescence images were acquired by epifluorescence microscopy using a 40X objective, and doxorubicin fluorescence was quantified using ImageJ software for about 100 cells per condition per experiment. Histograms are the mean ± SEM of 3 independent experiments. Significance is attained at P < 0.05.

Techniques Used: Expressing, Transfection, Negative Control, Western Blot, Software, Incubation, Control, Fluorescence, Epifluorescence Microscopy

Image Search Results

Journal: Translational Oncology

Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

doi: 10.1016/j.tranon.2026.102777

Figure Lengend Snippet: Ptch1 is expressed in breast cancer cell lines. A. PTCH1 mRNA expression (log 2 transformed) in various luminal and HER2 breast cancer cell lines (dark green) and in TNBC cell lines (other colors). TNBC cell lines are depicted according to the “Lehmann TNBC subtype” nomenclature : basal-like 1 (yellow), basal-like 2 (pale green), immunomodulatory (brown), luminal androgen receptor (dark pink), mesenchymal (pale pink) and mesenchymal stem-like (pink). B. PTCH1 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from TNBC cell lines (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against PTCH1. PTCH1 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*).

Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

Techniques: Expressing, Transformation Assay, Western Blot, Software

Journal: Translational Oncology

Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

doi: 10.1016/j.tranon.2026.102777

Figure Lengend Snippet: PTCH1 drug efflux inhibitor PAH increases the sensitivity of TNBC cells to chemotherapy . Cell viability was measured after 24 h or 48 h treatment with increasing concentration of docetaxel or doxorubicin respectively on MDA-MB-231, MDA-MB-468 and HCC-38 cell lines in the absence or the presence of 15µM PAH. IC 50 values (corresponding to the concentration of chemotherapy inducing 50% of cell death) were calculated. Data reported are the mean ± SEM of at least 3 independent experiments. Significance is attained at P < 0.05 (*).

Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

Techniques: Concentration Assay

Journal: Translational Oncology

Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

doi: 10.1016/j.tranon.2026.102777

Figure Lengend Snippet: Other multidrug transporters are expressed in TNBC cell lines. A. P-gp and ABCG2 protein expression in three TNBC cell lines. Western-blot was performed on 50 µg extracts from each TNBC cell line (MDA-MB-231, HCC-38 and MDA-MB-468) with antibodies directed against P-gp or ABCG2 and GAPDH. B. P-gp, ABCG2 and GAPDH signals were quantified using ImageJ software. Data presented are the mean ± SEM of at least 3 independent experiments. Significance is calculated using Oneway ANOVA Turkey’s multiple comparisons test and attained at P < 0.05 (*). ** P < 0.01; *** P < 0.001; ns P > 0.05.

Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

Techniques: Expressing, Western Blot, Software

Journal: Translational Oncology

Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

doi: 10.1016/j.tranon.2026.102777

Figure Lengend Snippet: PAH increases docetaxel efficacy against TNBC spheroids. MDA-MB-231 cells were plated in ultra-low attachment surface 24 well plates in complete medium and treated with increasing concentrations of docetaxel in the presence of DMSO (control, 0 PAH), PAH 10 µM or 30 µM. After 2 weeks pictures were taken using Cytation 5 cell imaging system from Biotek. The surface of spheroids was calculated and reported after normalization on the condition without docetaxel for each concentration of PAH.

Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

Techniques: Control, Imaging, Concentration Assay

Journal: Translational Oncology

Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

doi: 10.1016/j.tranon.2026.102777

Figure Lengend Snippet: PAH addition to chemotherapy inhibits migration of TNBC cells. A. 100000 cells were seeded on membrane from Transwell plates. Cells were treated 24 h with doxorubicin ± 15µM PAH or 48 h with docetaxel ± 15µM PAH. After fixation and staining with crystal violet, wells were observed on a microscope with X5 objective. B. Migration was measured using a wound-healing assay. A wound was performed on MDA-MB-231 confluent cells seeded in 24 well plates. The medium was replaced by fresh medium containing 5 µM docetaxel in the absence of PAH, or the presence of 5 µM PAH. Two pictures were taken at two different points of each well immediately after wound, and 3 days after wound with 5X objective. The width of the wound was measured using ImageJ software and reported as final wound width/initial wound width in percentage. Data presented are the mean ± SEM of 3 independent experiments. Significance is attained at P < 0.05.

Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

Techniques: Migration, Membrane, Staining, Microscopy, Wound Healing Assay, Software

Journal: Translational Oncology

Article Title: Inhibition of PTCH1 drug efflux activity enhances chemotherapy efficacy against triple negative breast cancers

doi: 10.1016/j.tranon.2026.102777

Figure Lengend Snippet: PTCH1 contributes to the efflux of doxorubicin from TNBC cells. A. PTCH1 protein expression (left panel) and intracellular doxorubicin (right panel) were analyzed 16 h after transfection of MDA-MB-231 cells with PTCH1-siRNA or negative-control-siRNA. PTCH1 and GAPDH western blot signals were quantified using ImageJ software (left panel). For doxorubicin accumulation measurements (right panel), MDA-MB-231 cells were grown on slides and transfected with PTCH1-siRNA or negative-control-siRNA. After incubation with 10 µM doxorubicin, 3 coverslips were fixed for doxorubicin loading control; the other coverslips were incubated with efflux buffer and fixed. B. Docetaxel inhibits the accumulation of doxorubicin in MDA-MB-231 cells. Cells on coverslip were incubated with 10 µM doxorubicin or 10 µM doxorubicin and 50 µM docetaxel. Doxorubicin fluorescence images were acquired by epifluorescence microscopy using a 40X objective, and doxorubicin fluorescence was quantified using ImageJ software for about 100 cells per condition per experiment. Histograms are the mean ± SEM of 3 independent experiments. Significance is attained at P < 0.05.

Article Snippet: Human breast cancer cell lines MDA-MB-231, MDA-MB-468 and HCC-38 were purchased from ATCC.

Techniques: Expressing, Transfection, Negative Control, Western Blot, Software, Incubation, Control, Fluorescence, Epifluorescence Microscopy

a) Design and location of CRISPR guide RNAs (pink and blue) and genotyping primers (yellow and green) targeting exon 1 of METTL3 b) Agarose gel showing the genotyping PCR products amplified from the CRISPR-Cas9 targeted region of a heterozygous knockout clone (HKO) and the parental cell line MDA-MB-468 (WT). c) Representation of METTL3 exon 1 of HKO showing the representative locations of CRISPR heterozygous deletions. d) qPCR analysis of METTL3 and METTL14 gene expression in WT and METTL3 HKO cells. P-value by one-way ANOVA followed by Tukey HSD post hoc multiple comparison test. e) Western blot analysis of METTL3, METTL14, VIRMA, RBM15 protein expression wild type and METTL3 +/− cells. Fibrillarin serves as a loading control. f) Western blot quantification of METTL3 on WT treated with 0.145µM STM2457 (n=3) or METTL3 HKO lines (n=3), compared to WT (n=3). Protein levels are represented as mean ratio values quantified from protein bands of METTL3 (lower band) versus Fibrillarin compared to WT. P-values calculated by one-way ANOVA followed by Tukey HSD post hoc multiple comparison test. g) m6A/A ratio of poly(A) purified mRNA as determined by LC–MS/MS in KO (n=2) and WT(n=2) cells.

Journal: bioRxiv

Article Title: Fine-tuning m6A and METTL3 levels have profound impact on cellular proliferation and protein synthesis

doi: 10.64898/2026.04.14.718245

Figure Lengend Snippet: a) Design and location of CRISPR guide RNAs (pink and blue) and genotyping primers (yellow and green) targeting exon 1 of METTL3 b) Agarose gel showing the genotyping PCR products amplified from the CRISPR-Cas9 targeted region of a heterozygous knockout clone (HKO) and the parental cell line MDA-MB-468 (WT). c) Representation of METTL3 exon 1 of HKO showing the representative locations of CRISPR heterozygous deletions. d) qPCR analysis of METTL3 and METTL14 gene expression in WT and METTL3 HKO cells. P-value by one-way ANOVA followed by Tukey HSD post hoc multiple comparison test. e) Western blot analysis of METTL3, METTL14, VIRMA, RBM15 protein expression wild type and METTL3 +/− cells. Fibrillarin serves as a loading control. f) Western blot quantification of METTL3 on WT treated with 0.145µM STM2457 (n=3) or METTL3 HKO lines (n=3), compared to WT (n=3). Protein levels are represented as mean ratio values quantified from protein bands of METTL3 (lower band) versus Fibrillarin compared to WT. P-values calculated by one-way ANOVA followed by Tukey HSD post hoc multiple comparison test. g) m6A/A ratio of poly(A) purified mRNA as determined by LC–MS/MS in KO (n=2) and WT(n=2) cells.

Article Snippet: Unless stated otherwise, MDA-MB-468 (obtained from ATCC (HTB-132)) and heterozygous knockout cell lines were maintained in DMEM containing 4.5g/L-glucose, L-Glutamine and sodium pyruvate (Thermo Fisher 41966-029), supplemented with 10% (v/v) foetal bovine serum and 1 % (v/v) penicillin/streptomycin at 37°C.

Techniques: CRISPR, Agarose Gel Electrophoresis, Amplification, Knock-Out, Gene Expression, Comparison, Western Blot, Expressing, Control, Purification, Liquid Chromatography with Mass Spectroscopy

a) Heatmap showing absolute area under the curve (AUC; 24–120 h) across co-treatment and glucose conditions (rows) and genotype or pretreatment (columns: WT, STM2457 3 µM, STM2120 3 µM, METTL3 heterozygous knockout [HKO], STM2457 0.145 µM). Asterisks indicate BH-FDR–adjusted significance relative to WT (*** ≤ 0.001; ** ≤ 0.01; * ≤ 0.05). b) Effect sizes (Cohen’s d) comparing STM2457 0.145 µM to WT across all conditions (red denotes FDR ≤ 0.05). c) Absolute growth curves (mean ± SEM) for MDA-MB-468 WT cells treated with STM2457 (3 µM or 0.145 µM), STM2120 (3 µM), or METTL3 HKO cells, cultured in 5.5 mM glucose. Together, panels (A–C) demonstrate that METTL3 HKO increases growth capacity relative to WT under mitogenic and nutrient-rich conditions, STM2457 3 µM suppresses growth capacity in STM-only and selected co-treatment contexts, and STM2457 0.145 µM produces modest effects relative to WT.

Journal: bioRxiv

Article Title: Fine-tuning m6A and METTL3 levels have profound impact on cellular proliferation and protein synthesis

doi: 10.64898/2026.04.14.718245

Figure Lengend Snippet: a) Heatmap showing absolute area under the curve (AUC; 24–120 h) across co-treatment and glucose conditions (rows) and genotype or pretreatment (columns: WT, STM2457 3 µM, STM2120 3 µM, METTL3 heterozygous knockout [HKO], STM2457 0.145 µM). Asterisks indicate BH-FDR–adjusted significance relative to WT (*** ≤ 0.001; ** ≤ 0.01; * ≤ 0.05). b) Effect sizes (Cohen’s d) comparing STM2457 0.145 µM to WT across all conditions (red denotes FDR ≤ 0.05). c) Absolute growth curves (mean ± SEM) for MDA-MB-468 WT cells treated with STM2457 (3 µM or 0.145 µM), STM2120 (3 µM), or METTL3 HKO cells, cultured in 5.5 mM glucose. Together, panels (A–C) demonstrate that METTL3 HKO increases growth capacity relative to WT under mitogenic and nutrient-rich conditions, STM2457 3 µM suppresses growth capacity in STM-only and selected co-treatment contexts, and STM2457 0.145 µM produces modest effects relative to WT.

Techniques: Knock-Out, Cell Culture

a) Volcano plots of differential protein abundance in MDA-MB-468 TNBC cells treated with STM2457 (0.145::JµM, 72::Jh) vs WT (MinProb; permutation. FDR::J<::J0.05; n ::J=::J3). b) Volcano plots for WT vs METTL3 heterozygous knockout (HKO) cells (as described above in a) . c) UpSet plot showing overlap of significantly differentially expressed proteins between drug-treated and METTL3 HKO cells. d) Heatmap of 2,097 significantly differentially expressed proteins (≥1 condition; FC::J>::J1; p ::J<::J0.05); red::J=::Jincrease, blue::J=::Jdecrease. e) Reactome pathway enrichment of significantly regulated leading-razor proteins (adj. p ::J<::J0.05; |log₂FC|::J≥::J1; Fisher’s exact test, perm. FDR::J<::J0.05). f) Venn diagram showing overlap of differentially methylated transcripts to steady-state protein changes (HKO vs WT). g) Top 20 enriched Gene Ontology (GO) biological process terms among genes showing both differential m6A methylation and protein expression changes.

Journal: bioRxiv

Article Title: Fine-tuning m6A and METTL3 levels have profound impact on cellular proliferation and protein synthesis

doi: 10.64898/2026.04.14.718245

Figure Lengend Snippet: a) Volcano plots of differential protein abundance in MDA-MB-468 TNBC cells treated with STM2457 (0.145::JµM, 72::Jh) vs WT (MinProb; permutation. FDR::J<::J0.05; n ::J=::J3). b) Volcano plots for WT vs METTL3 heterozygous knockout (HKO) cells (as described above in a) . c) UpSet plot showing overlap of significantly differentially expressed proteins between drug-treated and METTL3 HKO cells. d) Heatmap of 2,097 significantly differentially expressed proteins (≥1 condition; FC::J>::J1; p ::J<::J0.05); red::J=::Jincrease, blue::J=::Jdecrease. e) Reactome pathway enrichment of significantly regulated leading-razor proteins (adj. p ::J<::J0.05; |log₂FC|::J≥::J1; Fisher’s exact test, perm. FDR::J<::J0.05). f) Venn diagram showing overlap of differentially methylated transcripts to steady-state protein changes (HKO vs WT). g) Top 20 enriched Gene Ontology (GO) biological process terms among genes showing both differential m6A methylation and protein expression changes.

Techniques: Quantitative Proteomics, Knock-Out, Methylation, Expressing

a) Volcano plot showing differential phosphorylation of proteins in MDA-MB-468 cells treated with STM2457 (0.145::JµM, 72::Jh) compared to wild-type (WT) cells. Data were log₂-transformed, filtered for modified peptides, and imputed using MinProb (width = 0.3, shift = 1.8). Statistical analysis was performed using unpaired t-tests with permutation-based FDR correction (FDR < 0.05, fold change > 1, n = 3 biological replicates). b) Volcano plot comparing WT cells to METTL3 heterozygous knockout (HKO) cells under the same processing and statistical conditions as in a) . c) UpSet plot illustrating the overlap of significantly differentially phosphorylated proteins between STM2457-treated and METTL3 HKO cells. d) Heatmap of 2801 significantly differentially phosphorylated proteins detected by LC-MS in either STM2457-treated or METTL3 HKO cells compared to WT (significant in ≥1 condition; fold change > 1; p < 0.05). Red indicates increased phosphorylation; blue indicates decreased phosphorylation. All conditions include 3 biological replicates. e) Reactome pathway enrichment of proteins undergoing differential phosphorylation upon partial reduction of METTL3 abundance or activity. Only conditions with more than one significantly enriched ontology term (adjusted p-value < 0.05, ≥2 proteins per term) are shown.

Journal: bioRxiv

Article Title: Fine-tuning m6A and METTL3 levels have profound impact on cellular proliferation and protein synthesis

doi: 10.64898/2026.04.14.718245

Figure Lengend Snippet: a) Volcano plot showing differential phosphorylation of proteins in MDA-MB-468 cells treated with STM2457 (0.145::JµM, 72::Jh) compared to wild-type (WT) cells. Data were log₂-transformed, filtered for modified peptides, and imputed using MinProb (width = 0.3, shift = 1.8). Statistical analysis was performed using unpaired t-tests with permutation-based FDR correction (FDR < 0.05, fold change > 1, n = 3 biological replicates). b) Volcano plot comparing WT cells to METTL3 heterozygous knockout (HKO) cells under the same processing and statistical conditions as in a) . c) UpSet plot illustrating the overlap of significantly differentially phosphorylated proteins between STM2457-treated and METTL3 HKO cells. d) Heatmap of 2801 significantly differentially phosphorylated proteins detected by LC-MS in either STM2457-treated or METTL3 HKO cells compared to WT (significant in ≥1 condition; fold change > 1; p < 0.05). Red indicates increased phosphorylation; blue indicates decreased phosphorylation. All conditions include 3 biological replicates. e) Reactome pathway enrichment of proteins undergoing differential phosphorylation upon partial reduction of METTL3 abundance or activity. Only conditions with more than one significantly enriched ontology term (adjusted p-value < 0.05, ≥2 proteins per term) are shown.

Techniques: Phospho-proteomics, Transformation Assay, Modification, Knock-Out, Liquid Chromatography with Mass Spectroscopy, Activity Assay

Estrogen- GRK2 pathway and its functional implications in TNBC chemoresistance. A Volcano plot showing enriched PTM pathways between the pCR and non-pCR groups by PTM-SEA. The x-axis represents the NES, and the y-axis shows the -log 10 ( p -value). Only pathways meeting the significance threshold (|NES|> 5 and p -value < 0.05) are color-coded (red: NES > 5 and blue: NES < −5), whereas nonsignificant pathways are shown in gray. B Correlation analysis between the GRK2 PTM-SEA NES and early estrogen response GSVA scores. C Correlation analysis between the GRK2 PTM-SEA NES and late estrogen response GSVA scores. D Correlation analysis between the GRK2 PTM-SEA NES and ESTIMATE immune scores. E Heatmap of in vitro kinase-to-phosphosite database (iKiP) GRK2 pathway-associated phosphosites used in the PTM-SEA analysis. Asterisks (*) denote statistically significant differences ( P < 0.05) between the pCR and non-pCR group. F GSVA comparison of Hallmark pathways between GRK2 PTM-SEA score–high and score–low tumors. Estrogen response early ( P = 0.0324) and allograft rejection ( P = 0.0310) were significantly different, with estrogen response early and late pathways enriched in the GRK2-high group, whereas allograft rejection and interferon alpha/gamma response were higher in the GRK2-low group. Data are presented as mean ± SD. G Immunoblot showing GRK2 protein expression on estradiol treatment for 24 h in MDA-MB468 cell line. Protein size markers were indicated on the right side of the immunoblots. H Dose–response curve of relative proliferation of MDA-MB231 cells treated with paclitaxel and GRK2 inhibitor (βARK inhibitor, 4 μg/ml [15.2 nM]) plus paclitaxel in the in-vitro 3-(4,5-dimethylthiazol-2-yl)−2,5-diphenyltetrazolium bromide (MTT) assay. The x-axis is log 10 (paclitaxel concentration). The results are from three biologic replicates, and the error bars indicate the standard error of the mean (SEM). * P < 0.05 by Student’s t test with Welch’s adjustment for heteroscedasticity (E) or by Pearson’s correlation (B, C, and D). See also Figure S8. GRK2i, GRK2 inhibitor; GSVA, gene set variation analysis; iKiP, in vitro kinase-to-phosphosite; NES, normalized enrichment score; pCR, pathological complete response; PTM, post-translational modification; PTM-SEA, post-translational modification set enrichment analysis

Journal: Genome Biology

Article Title: Proteogenomic decoding of chemotherapy resistance in patients with triple-negative breast cancer

doi: 10.1186/s13059-026-04053-7

Figure Lengend Snippet: Estrogen- GRK2 pathway and its functional implications in TNBC chemoresistance. A Volcano plot showing enriched PTM pathways between the pCR and non-pCR groups by PTM-SEA. The x-axis represents the NES, and the y-axis shows the -log 10 ( p -value). Only pathways meeting the significance threshold (|NES|> 5 and p -value < 0.05) are color-coded (red: NES > 5 and blue: NES < −5), whereas nonsignificant pathways are shown in gray. B Correlation analysis between the GRK2 PTM-SEA NES and early estrogen response GSVA scores. C Correlation analysis between the GRK2 PTM-SEA NES and late estrogen response GSVA scores. D Correlation analysis between the GRK2 PTM-SEA NES and ESTIMATE immune scores. E Heatmap of in vitro kinase-to-phosphosite database (iKiP) GRK2 pathway-associated phosphosites used in the PTM-SEA analysis. Asterisks (*) denote statistically significant differences ( P < 0.05) between the pCR and non-pCR group. F GSVA comparison of Hallmark pathways between GRK2 PTM-SEA score–high and score–low tumors. Estrogen response early ( P = 0.0324) and allograft rejection ( P = 0.0310) were significantly different, with estrogen response early and late pathways enriched in the GRK2-high group, whereas allograft rejection and interferon alpha/gamma response were higher in the GRK2-low group. Data are presented as mean ± SD. G Immunoblot showing GRK2 protein expression on estradiol treatment for 24 h in MDA-MB468 cell line. Protein size markers were indicated on the right side of the immunoblots. H Dose–response curve of relative proliferation of MDA-MB231 cells treated with paclitaxel and GRK2 inhibitor (βARK inhibitor, 4 μg/ml [15.2 nM]) plus paclitaxel in the in-vitro 3-(4,5-dimethylthiazol-2-yl)−2,5-diphenyltetrazolium bromide (MTT) assay. The x-axis is log 10 (paclitaxel concentration). The results are from three biologic replicates, and the error bars indicate the standard error of the mean (SEM). * P < 0.05 by Student’s t test with Welch’s adjustment for heteroscedasticity (E) or by Pearson’s correlation (B, C, and D). See also Figure S8. GRK2i, GRK2 inhibitor; GSVA, gene set variation analysis; iKiP, in vitro kinase-to-phosphosite; NES, normalized enrichment score; pCR, pathological complete response; PTM, post-translational modification; PTM-SEA, post-translational modification set enrichment analysis

Article Snippet: The TNBC cell lines, including MDA-MB-231 (HTB-26), MDA-MB-468 (HTB-132), and HCC1937 (CRL-2336), were purchased from the ATCC.

Techniques: Functional Assay, In Vitro, Phospho-proteomics, Comparison, Western Blot, Expressing, MTT Assay, Concentration Assay, Modification

Identification of chemotherapy resistance mechanisms in the IM subtype and baseline and post-treatment tumor comparison. A Volcano plot showing differentially expressed mRNAs between non-pCR and pCR tumors in the Lehmann classification IM subtype. B Violin plot showing mRNA expression levels of AKR1C2 and ABCA13 stratified by the five NMF clusters. C Heatmap comparing mRNA expression of xenobiotic metabolism genes across the TNBC cohort. D Hallmark pathway enrichment analysis comparing baseline versus post-treatment samples using phosphoproteomic and global proteomic data. Pathways are plotted according to their − log₁₀(FDR) values derived from GSEA of phosphoprotein expression (x-axis) and protein expression (y-axis). Pathways enriched in the post-treatment group are shown on the positive axis (phosphoprotein: right on the x-axis; protein: up on the y-axis), whereas those enriched in the baseline group appear on the negative axis (phosphoprotein: left on the x-axis; protein: down on the y-axis). Significance is represented by − log₁₀(FDR); color indicates statistical significance in the protein layer only (orange) or in both phosphoprotein and protein layers (blue). E Bar plot showing the enriched Hallmark pathways in DEGs between post-treatment and baseline samples in global protein expression data. The top five gene signatures are described. F Volcano plot showing enriched PTM signatures in baseline versus post-treatment tumor samples via the PTM-SEA analysis. G Dose–response curve of relative proliferation of MDA-MB468 cells treated with paclitaxel and barasertib (Aurora kinase B inhibitor, 10 nM) plus paclitaxel in the in-vitro MTT assay. The x-axis is log 10 (paclitaxel concentration). The results are from three biologic replicates, and the error bars indicate SEM. See also Figure S12. GSEA, gene set enrichment analysis; NMF, non-negative matrix factorization; pCR, pathological complete response; PTM, post-translational modification; TMT, tandem mass tag

Journal: Genome Biology

Article Title: Proteogenomic decoding of chemotherapy resistance in patients with triple-negative breast cancer

doi: 10.1186/s13059-026-04053-7

Figure Lengend Snippet: Identification of chemotherapy resistance mechanisms in the IM subtype and baseline and post-treatment tumor comparison. A Volcano plot showing differentially expressed mRNAs between non-pCR and pCR tumors in the Lehmann classification IM subtype. B Violin plot showing mRNA expression levels of AKR1C2 and ABCA13 stratified by the five NMF clusters. C Heatmap comparing mRNA expression of xenobiotic metabolism genes across the TNBC cohort. D Hallmark pathway enrichment analysis comparing baseline versus post-treatment samples using phosphoproteomic and global proteomic data. Pathways are plotted according to their − log₁₀(FDR) values derived from GSEA of phosphoprotein expression (x-axis) and protein expression (y-axis). Pathways enriched in the post-treatment group are shown on the positive axis (phosphoprotein: right on the x-axis; protein: up on the y-axis), whereas those enriched in the baseline group appear on the negative axis (phosphoprotein: left on the x-axis; protein: down on the y-axis). Significance is represented by − log₁₀(FDR); color indicates statistical significance in the protein layer only (orange) or in both phosphoprotein and protein layers (blue). E Bar plot showing the enriched Hallmark pathways in DEGs between post-treatment and baseline samples in global protein expression data. The top five gene signatures are described. F Volcano plot showing enriched PTM signatures in baseline versus post-treatment tumor samples via the PTM-SEA analysis. G Dose–response curve of relative proliferation of MDA-MB468 cells treated with paclitaxel and barasertib (Aurora kinase B inhibitor, 10 nM) plus paclitaxel in the in-vitro MTT assay. The x-axis is log 10 (paclitaxel concentration). The results are from three biologic replicates, and the error bars indicate SEM. See also Figure S12. GSEA, gene set enrichment analysis; NMF, non-negative matrix factorization; pCR, pathological complete response; PTM, post-translational modification; TMT, tandem mass tag

Article Snippet: The TNBC cell lines, including MDA-MB-231 (HTB-26), MDA-MB-468 (HTB-132), and HCC1937 (CRL-2336), were purchased from the ATCC.

Techniques: Comparison, Expressing, Derivative Assay, In Vitro, MTT Assay, Concentration Assay, Modification

Venn diagrams depicting the intersection of upregulated DEGs from MDA-MB-231 vs. MCF7 comparison (GEO datasets GSE210306 and GSE222313 ) with putative targets of miR-205-5p ( A ), miR-141-3p ( B ) and miR-200c-3p ( C ).

Journal: Biology

Article Title: Bioinformatics Analysis of microRNAs Associated with Metastatic Potential in Breast Cancer

doi: 10.3390/biology15080617

Figure Lengend Snippet: Venn diagrams depicting the intersection of upregulated DEGs from MDA-MB-231 vs. MCF7 comparison (GEO datasets GSE210306 and GSE222313 ) with putative targets of miR-205-5p ( A ), miR-141-3p ( B ) and miR-200c-3p ( C ).

Article Snippet: ER-positive MCF7 cells and triple-negative BC cell lines MDA-MB-231 and MDA-MB-468 were obtained from the American Type Culture Collection (Rockville, MD, USA).

Techniques: Comparison

Cancer hallmark enrichment graphs for upregulated DEGs from MDA-MB-231 vs. MCF7 comparison (GEO datasets GSE210306 and GSE222313 ) within putative target lists of miR-205-5p ( A ), miR-141-3p ( B ) and miR-200c-3p ( C ). Red circles represent statistical significance threshold.

Journal: Biology

Article Title: Bioinformatics Analysis of microRNAs Associated with Metastatic Potential in Breast Cancer

doi: 10.3390/biology15080617

Figure Lengend Snippet: Cancer hallmark enrichment graphs for upregulated DEGs from MDA-MB-231 vs. MCF7 comparison (GEO datasets GSE210306 and GSE222313 ) within putative target lists of miR-205-5p ( A ), miR-141-3p ( B ) and miR-200c-3p ( C ). Red circles represent statistical significance threshold.

Article Snippet: ER-positive MCF7 cells and triple-negative BC cell lines MDA-MB-231 and MDA-MB-468 were obtained from the American Type Culture Collection (Rockville, MD, USA).

Techniques: Comparison

Relative expression of putative DE-microRNAs in MCF7 and TNBC cell lines MDA-MB-231 and MDA-MB-468. Bar plots represent mean fold changes, relative to MCF7 cells + SD; p < 0.01 is indicated by two asterisks and p < 0.001 by three asterisks.

Journal: Biology

Article Title: Bioinformatics Analysis of microRNAs Associated with Metastatic Potential in Breast Cancer

doi: 10.3390/biology15080617

Figure Lengend Snippet: Relative expression of putative DE-microRNAs in MCF7 and TNBC cell lines MDA-MB-231 and MDA-MB-468. Bar plots represent mean fold changes, relative to MCF7 cells + SD; p < 0.01 is indicated by two asterisks and p < 0.001 by three asterisks.

Article Snippet: ER-positive MCF7 cells and triple-negative BC cell lines MDA-MB-231 and MDA-MB-468 were obtained from the American Type Culture Collection (Rockville, MD, USA).

Techniques: Expressing

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