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ATCC human tnbc cell lines mda mb 231
Human Tnbc Cell Lines Mda Mb 231, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 24477 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 99 stars, based on 24477 article reviews

human tnbc cell lines mda mb 231 - by Bioz Stars, 2026-09

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Cell viability of the cell lines MCF-10A (A), MCF-7 (B), and MDA-MB-231 (C) after treatments with IsCT1 (green bars) or AKFK-IsCT1 (purple bars) at concentrations up to 4.0 μM, followed by incubation at 37 °C and 5% CO 2 for 4 h. Green bars represent IsCT1, and pink bars represent AKFK-IsCT1. Data are expressed as mean ± SD of three independent experiments performed in triplicate. Statistical significance was determined using two-way ANOVA followed by Tukey test, ** p < 0.005; **** p < 0.0001.

Journal: ACS Pharmacology & Translational Science

Article Title: Engineering the Host Defense Peptide from Scorpion Venom for Safer and More Potent Antibreast Cancer Activity

doi: 10.1021/acsptsci.5c00598

Figure Lengend Snippet: Cell viability of the cell lines MCF-10A (A), MCF-7 (B), and MDA-MB-231 (C) after treatments with IsCT1 (green bars) or AKFK-IsCT1 (purple bars) at concentrations up to 4.0 μM, followed by incubation at 37 °C and 5% CO 2 for 4 h. Green bars represent IsCT1, and pink bars represent AKFK-IsCT1. Data are expressed as mean ± SD of three independent experiments performed in triplicate. Statistical significance was determined using two-way ANOVA followed by Tukey test, ** p < 0.005; **** p < 0.0001.

Article Snippet: The triple-negative breast cancer (TNBC) cell lines human MDA-MB-231 (CRM-HTB-26) and murine 4T1 (CRL-2539), human adenocarcinoma cell line MCF-7 (HTB-22), and the human breast epithelial cell line MCF-10A (CRL-10317) were obtained from American Type Culture Collection (ATCC).

Techniques: Incubation

Cell viability after combined treatment with photodynamic therapy using hypericin (PDT-Hyp, 0.05 μM) and peptides under two treatment protocols. Protocol 1 (PDT-Hyp followed by peptide exposure) was applied to (A) MCF-10A, (B) MCF-7, and (C) MDA-MB-231 cells, whereas Protocol 2 (peptide exposure followed by PDT-Hyp) was applied to (D) MCF-10A, (E) MCF-7, and (F) MDA-MB-231 cells. Blue bars represent IsCT1, and red bars represent AKFK-IsCT1. Peptides were tested at concentrations ranging from 0.01 to 4.0 μM. Cells were incubated at 37 °C and 5% CO 2 for 4 h following treatment. Data are expressed as mean ± SD of three independent experiments performed in triplicate. Statistical significance was determined using two-way ANOVA followed by Tukey test, * p < 0.05; ** p < 0.005; *** p < 0.0005; **** p < 0.0001.

Journal: ACS Pharmacology & Translational Science

Article Title: Engineering the Host Defense Peptide from Scorpion Venom for Safer and More Potent Antibreast Cancer Activity

doi: 10.1021/acsptsci.5c00598

Figure Lengend Snippet: Cell viability after combined treatment with photodynamic therapy using hypericin (PDT-Hyp, 0.05 μM) and peptides under two treatment protocols. Protocol 1 (PDT-Hyp followed by peptide exposure) was applied to (A) MCF-10A, (B) MCF-7, and (C) MDA-MB-231 cells, whereas Protocol 2 (peptide exposure followed by PDT-Hyp) was applied to (D) MCF-10A, (E) MCF-7, and (F) MDA-MB-231 cells. Blue bars represent IsCT1, and red bars represent AKFK-IsCT1. Peptides were tested at concentrations ranging from 0.01 to 4.0 μM. Cells were incubated at 37 °C and 5% CO 2 for 4 h following treatment. Data are expressed as mean ± SD of three independent experiments performed in triplicate. Statistical significance was determined using two-way ANOVA followed by Tukey test, * p < 0.05; ** p < 0.005; *** p < 0.0005; **** p < 0.0001.

Techniques: Incubation

Three-dimensional Bliss synergy response surfaces for the combined treatment of PDT-Hyp and peptides applied under different treatment protocols. Protocol 1 was evaluated with IsCT1 (A, E, I) or AKFK-IsCT1 (C, G, K), whereas Protocol 2 was evaluated with IsCT1 (B, F, J) or AKFK-IsCT1 (D, H, L). Panels in the first row (A–D) correspond to MCF-10A cells, the second row (E–H) to MCF-7 cells, and the third row (I–L) to MDA-MB-231 cells. Color coding represents Bliss synergy scores, where green indicates antagonism (≤0), intermediate colors between white and light red indicate additive effects (>0 and ≤10), and red indicates synergistic interactions (>10). Color intensity is proportional to the magnitude of the interaction score. Bliss synergy scores and response surfaces were generated from complete dose–response matrices using SynergyFinder 3.0.

Journal: ACS Pharmacology & Translational Science

Article Title: Engineering the Host Defense Peptide from Scorpion Venom for Safer and More Potent Antibreast Cancer Activity

doi: 10.1021/acsptsci.5c00598

Figure Lengend Snippet: Three-dimensional Bliss synergy response surfaces for the combined treatment of PDT-Hyp and peptides applied under different treatment protocols. Protocol 1 was evaluated with IsCT1 (A, E, I) or AKFK-IsCT1 (C, G, K), whereas Protocol 2 was evaluated with IsCT1 (B, F, J) or AKFK-IsCT1 (D, H, L). Panels in the first row (A–D) correspond to MCF-10A cells, the second row (E–H) to MCF-7 cells, and the third row (I–L) to MDA-MB-231 cells. Color coding represents Bliss synergy scores, where green indicates antagonism (≤0), intermediate colors between white and light red indicate additive effects (>0 and ≤10), and red indicates synergistic interactions (>10). Color intensity is proportional to the magnitude of the interaction score. Bliss synergy scores and response surfaces were generated from complete dose–response matrices using SynergyFinder 3.0.

Techniques: Generated

Brain pericyte secretions mediate the inhibition of TNBC cell adhesion to the BBB. (A) Experimental workflow for adhesion assay. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. The astrocyte medium was renewed 24 h before the adhesion experiment with the same ECGMV2 medium. Endothelial cells (ECs) and brain pericytes (hBPs) were co‐cultured for 5 days, and inserts containing brain‐like endothelial cells (hBLECs) were then either maintained with hBPs or transferred to wells without hBPs. After 24 hours, and prior to MDA‐MB‐231 cells seeding, inserts were subjected to the following conditions: maintained without hBPs (hBLEC 24h); transferred to hBPs previously cultured alone for 24 hours (hBLEC 24h then hBP); transferred to wells without hBPs but containing either culture medium (hBLEC) or CM from co‐culture (hBLEC + CM coc ); transferred to wells with astrocytes (hBLEC + A) or maintained in co‐culture with hBPs (hBLEC + hBP). (B–G), Quantification (B, D, F) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E, G) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (B), Welch's ANOVA followed by Dunnett's T3 test (D) and Kruskal–Wallis test followed by Dunn's test (F). CM coc = conditioned medium from 24 h hBLECs and hBPs coculture, A = astrocytes, hBP mono = 24 h hBPs monoculture. Scale bar = 750 µm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; ECs, endothelial cells; hBLECs, human brain‐like endothelial cells; ns, non‐significant; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericyte secretions mediate the inhibition of TNBC cell adhesion to the BBB. (A) Experimental workflow for adhesion assay. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. The astrocyte medium was renewed 24 h before the adhesion experiment with the same ECGMV2 medium. Endothelial cells (ECs) and brain pericytes (hBPs) were co‐cultured for 5 days, and inserts containing brain‐like endothelial cells (hBLECs) were then either maintained with hBPs or transferred to wells without hBPs. After 24 hours, and prior to MDA‐MB‐231 cells seeding, inserts were subjected to the following conditions: maintained without hBPs (hBLEC 24h); transferred to hBPs previously cultured alone for 24 hours (hBLEC 24h then hBP); transferred to wells without hBPs but containing either culture medium (hBLEC) or CM from co‐culture (hBLEC + CM coc ); transferred to wells with astrocytes (hBLEC + A) or maintained in co‐culture with hBPs (hBLEC + hBP). (B–G), Quantification (B, D, F) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E, G) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (B), Welch's ANOVA followed by Dunnett's T3 test (D) and Kruskal–Wallis test followed by Dunn's test (F). CM coc = conditioned medium from 24 h hBLECs and hBPs coculture, A = astrocytes, hBP mono = 24 h hBPs monoculture. Scale bar = 750 µm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; ECs, endothelial cells; hBLECs, human brain‐like endothelial cells; ns, non‐significant; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Inhibition, Cell Adhesion Assay, Cell Culture, Co-Culture Assay, Incubation

Brain pericytes maintain BBB integrity in the presence of TNBC cells. (A–E) Endothelial permeability (Pe) to Lucifer Yellow assessed after 3 h (A) or 16 h (C) of incubation with MDA‐MB‐231 cells, in the presence or absence of brain pericytes (hBPs). Permeability was also measured in the absence of cancer cells as a control. Permeability values (expressed in × 10 −3 cm/min ± SD) are summarized in a table (E). Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h (B) or 16 h (D) of incubation with MDA‐MB‐231 cells (green). Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (A) and Welch's ANOVA followed by Dunnett's T3 test (B). MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes maintain BBB integrity in the presence of TNBC cells. (A–E) Endothelial permeability (Pe) to Lucifer Yellow assessed after 3 h (A) or 16 h (C) of incubation with MDA‐MB‐231 cells, in the presence or absence of brain pericytes (hBPs). Permeability was also measured in the absence of cancer cells as a control. Permeability values (expressed in × 10 −3 cm/min ± SD) are summarized in a table (E). Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h (B) or 16 h (D) of incubation with MDA‐MB‐231 cells (green). Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (A) and Welch's ANOVA followed by Dunnett's T3 test (B). MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Permeability, Incubation, Control, Immunostaining

Brain pericytes limit TNBC cell adhesion to the BBB under hypoxic conditions. (A) Experimental workflow for adhesion assay in hypoxic conditions. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. After 5 days of co‐culture with brain pericytes (hBPs), inserts containing brain‐like endothelial cells (hBLECs) were exposed to hypoxia for 24 h in the presence or absence of hBPs. Parallel conditions maintained in normoxia served as controls. (B–E) Quantification (B, D) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test (B) and Kruskal‐Wallis test followed by Dunn's test (D). hBP‐CM mono = conditioned medium from 24 h hBPs monoculture. Scale bar = 750 μm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes limit TNBC cell adhesion to the BBB under hypoxic conditions. (A) Experimental workflow for adhesion assay in hypoxic conditions. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. After 5 days of co‐culture with brain pericytes (hBPs), inserts containing brain‐like endothelial cells (hBLECs) were exposed to hypoxia for 24 h in the presence or absence of hBPs. Parallel conditions maintained in normoxia served as controls. (B–E) Quantification (B, D) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test (B) and Kruskal‐Wallis test followed by Dunn's test (D). hBP‐CM mono = conditioned medium from 24 h hBPs monoculture. Scale bar = 750 μm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Cell Adhesion Assay, Co-Culture Assay, Incubation

Brain pericytes maintain BBB integrity in the presence of TNBC cells under hypoxic conditions and supplement deprivation. (A) After 5 days of co‐culture with brain pericytes (hBPs) in ECGMV2 medium with supplements, inserts containing brain‐like endothelial cells (hBLECs) co‐cultured with hBPs were exposed to hypoxia for 16 h following medium replacement with ECGMV2 basal medium (without supplements). Then, endothelial permeability (Pe) to Lucifer Yellow was assessed after 3 h of incubation with MDA‐MB‐231 cells, in the presence or absence of hBPs, under normoxic and hypoxic conditions. (B) Permeability values (expressed in x10 −3 cm/min ± SD) are summarized in a table. (C) Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h of incubation with MDA‐MB‐231 cells (green) under hypoxic conditions in basal medium. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test. MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes maintain BBB integrity in the presence of TNBC cells under hypoxic conditions and supplement deprivation. (A) After 5 days of co‐culture with brain pericytes (hBPs) in ECGMV2 medium with supplements, inserts containing brain‐like endothelial cells (hBLECs) co‐cultured with hBPs were exposed to hypoxia for 16 h following medium replacement with ECGMV2 basal medium (without supplements). Then, endothelial permeability (Pe) to Lucifer Yellow was assessed after 3 h of incubation with MDA‐MB‐231 cells, in the presence or absence of hBPs, under normoxic and hypoxic conditions. (B) Permeability values (expressed in x10 −3 cm/min ± SD) are summarized in a table. (C) Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h of incubation with MDA‐MB‐231 cells (green) under hypoxic conditions in basal medium. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test. MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Co-Culture Assay, Cell Culture, Permeability, Incubation, Immunostaining

Brain pericytes enhance migratory and invasion properties of TNBC cells. (A) Quantification of MDA‐MB‐231 cells that migrated to the lower side of insert filters in the absence (∅) or presence of brain pericytes (+hBPs), and representative images of migrated cells (nuclei stained in blue) associated. (B) Quantification of MDA‐MB‐231 cells that invaded the lower side of insert filters pre‐coated with Matrigel ® in the presence (+hBP) or absence (∅) of hBPs. (C) Representative images of MDA‐MB‐231 cells (green) after 48 h of monoculture or co‐culture with hBPs; cell morphology is visualized by F‐actin staining (phalloidin, orange). (D) Heatmap visualization of F‐actin intensity. (E) Quantification of cortical F‐actin fluorescence in MDA‐MB‐231 cells. (F) MDA‐MB‐231 cell elongation factor, defined as the ratio of cell length to width, following 48 h of monoculture (MDA) and co‐culture with hBPs (MDA + hBP), or following 1‐hour treatment with DMEM 0.1% (CTL medium) and hBP‐CM. Data are obtained from three independent experiments, with three technical replicates (A, B) or at least 30 cells analyzed (E, F) per condition. Statistical analyses were performed using a Mann–Whitney test (A, E, F) and an unpaired t ‐test with Welch's correction (B). MDA = MDA‐MB‐231 cells. Scale bars = 750 μm (A) and 100 μm (C, D). DMEM, Dulbecco'’s Modified Eagle Medium; hBP‐CM, hBP‐conditioned medium; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes enhance migratory and invasion properties of TNBC cells. (A) Quantification of MDA‐MB‐231 cells that migrated to the lower side of insert filters in the absence (∅) or presence of brain pericytes (+hBPs), and representative images of migrated cells (nuclei stained in blue) associated. (B) Quantification of MDA‐MB‐231 cells that invaded the lower side of insert filters pre‐coated with Matrigel ® in the presence (+hBP) or absence (∅) of hBPs. (C) Representative images of MDA‐MB‐231 cells (green) after 48 h of monoculture or co‐culture with hBPs; cell morphology is visualized by F‐actin staining (phalloidin, orange). (D) Heatmap visualization of F‐actin intensity. (E) Quantification of cortical F‐actin fluorescence in MDA‐MB‐231 cells. (F) MDA‐MB‐231 cell elongation factor, defined as the ratio of cell length to width, following 48 h of monoculture (MDA) and co‐culture with hBPs (MDA + hBP), or following 1‐hour treatment with DMEM 0.1% (CTL medium) and hBP‐CM. Data are obtained from three independent experiments, with three technical replicates (A, B) or at least 30 cells analyzed (E, F) per condition. Statistical analyses were performed using a Mann–Whitney test (A, E, F) and an unpaired t ‐test with Welch's correction (B). MDA = MDA‐MB‐231 cells. Scale bars = 750 μm (A) and 100 μm (C, D). DMEM, Dulbecco'’s Modified Eagle Medium; hBP‐CM, hBP‐conditioned medium; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Staining, Co-Culture Assay, Fluorescence, MANN-WHITNEY, Modification

Brain pericyte secretions enhance TNBC clonogenic capacity. (A) Representative images of MDA‐MB‐231 colony formation following exposure to conditioned medium from brain pericytes (hBP‐CM), control medium (DMEM 0.1%, medium used for CM generation), or DMEM 10%. (B) Quantification of colony numbers formed by MDA‐MB‐231 under previously indicated conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using a Mann–Whitney test. MDA = MDA‐MB‐231 cells. Scale bar = 600 μm. DMEM, Dulbecco'’s Modified Eagle Medium; hBP‐CM, hBP‐conditioned medium; TNBC, triple‐negative breast cancer.

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericyte secretions enhance TNBC clonogenic capacity. (A) Representative images of MDA‐MB‐231 colony formation following exposure to conditioned medium from brain pericytes (hBP‐CM), control medium (DMEM 0.1%, medium used for CM generation), or DMEM 10%. (B) Quantification of colony numbers formed by MDA‐MB‐231 under previously indicated conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using a Mann–Whitney test. MDA = MDA‐MB‐231 cells. Scale bar = 600 μm. DMEM, Dulbecco'’s Modified Eagle Medium; hBP‐CM, hBP‐conditioned medium; TNBC, triple‐negative breast cancer.

Article Snippet: The human TNBC cell line MDA‐MB‐231 (female) was obtained from the American type culture collection (ATCC, HTB‐26, RRID:CVCL_0062, obtained in 2023).

Techniques: Control, MANN-WHITNEY, Modification

Metabolome characterization of TNBC cells after irradiation. A Workflow of untargeted metabolomics in irradiated cells. Image created with BioRender.com. B Partial Least-Squares Discriminant Analysis (PLS-DA) on metabolome dataset from MDA-MB-231 cells created using MetaboAnalyst.ca web tool. C LC-MS/MS analytical feature processing for metabolite prediction using Human Metabolome Data Base (HMDB) web tool. D Classification of metabolites into their respective categories using HMDB. E Identification of radiation-induced changes in metabolites categorized by color-coded groups. Data are presented as mean ( n = 6) fold change relative to control, with significance determined by t-test ( p < 0.05) in MetaboAnalyst.ca. Circles indicate the number of up- and downregulated metabolites in the respective category. F Impact of irradiation on metabolic pathways in TNBC cells. Corresponding p-values are aligned with the percentage of altered metabolites relative to all metabolites found in the indicated pathway. Data obtained from MetaboAnalyst.ca, Kyoto Encyclopedia of Genes and Genomes (KEGG), and Small Molecule Pathway Data Base (SMPDB) databases. G Relative abundance of metabolites altered in irradiated cells within the indicated metabolic pathways, presented as a mean ± SEM ( n = 6) fold change relative to the control. H Metabolite-metabolite interaction network of metabolites altered in irradiated cells relative to controls, generated in MetaboAnalyst.ca

Journal: Cell Communication and Signaling : CCS

Article Title: Precise metabolomics identifies glycolysis-related pyruvate kinase M activity as regulator of the S-phase-specific radiation response in triple-negative breast cancer cells

doi: 10.1186/s12964-026-02803-5

Figure Lengend Snippet: Metabolome characterization of TNBC cells after irradiation. A Workflow of untargeted metabolomics in irradiated cells. Image created with BioRender.com. B Partial Least-Squares Discriminant Analysis (PLS-DA) on metabolome dataset from MDA-MB-231 cells created using MetaboAnalyst.ca web tool. C LC-MS/MS analytical feature processing for metabolite prediction using Human Metabolome Data Base (HMDB) web tool. D Classification of metabolites into their respective categories using HMDB. E Identification of radiation-induced changes in metabolites categorized by color-coded groups. Data are presented as mean ( n = 6) fold change relative to control, with significance determined by t-test ( p < 0.05) in MetaboAnalyst.ca. Circles indicate the number of up- and downregulated metabolites in the respective category. F Impact of irradiation on metabolic pathways in TNBC cells. Corresponding p-values are aligned with the percentage of altered metabolites relative to all metabolites found in the indicated pathway. Data obtained from MetaboAnalyst.ca, Kyoto Encyclopedia of Genes and Genomes (KEGG), and Small Molecule Pathway Data Base (SMPDB) databases. G Relative abundance of metabolites altered in irradiated cells within the indicated metabolic pathways, presented as a mean ± SEM ( n = 6) fold change relative to the control. H Metabolite-metabolite interaction network of metabolites altered in irradiated cells relative to controls, generated in MetaboAnalyst.ca

Article Snippet: Human TNBC cell lines: MDA-MB-231, purchased from American Type Tissue Culture Collection (ATCC, HTB-26) (Manassas, VA, USA), Cal-85-1 (ACC 440), Cal-51 (ACC 302), both purchased from DSMZ, MDA-MB-468, Hs 578T, and BT-549 (kindly provided by S. Joosse; University Medical Center Hamburg-Eppendorf, Hamburg, Germany).

Techniques: Irradiation, Liquid Chromatography with Mass Spectroscopy, Control, Generated

Identification of PKM as the most promising target for radiosensitization in TNBC cells. A Workflow illustrating the discovery of druggable candidates by database gene filtering on radiation-induced metabolic alterations. Image created with BioRender.com. B Venn diagram depicting the selection of metabolite-interacting genes through database alignment. C Gene filtering for the selection of potential therapeutic targets based on the indicated criteria. D Clonogenic basal survival (0 Gy) or clonogenic radiation survival (6 Gy) of MDA-MB-231 cells depleted of indicated candidates. Data are presented as enhancement ratios relative to non-specific siRNA controls, represented as mean ( n = 4), and colored based on significance (p-value) calculated by one-way ANOVA. E Combination of the target-specific inhibitors (IC 50 ) with irradiation (IR) in MDA-MB-231 cells ( n = 3). Results show mean ± SEM. Statistical significance was determined by unpaired two-tailed Student’s t-test and indicated as * p < 0.05; ** p < 0.01, or ns = not significant. F Kaplan-Meier analyses based on the mRNA expression of the indicated candidate genes using the METABRIC-TNBC patient cohort. 10-year overall survival (OS) curves show the highest vs. the lowest mRNA expression quartiles, the confidence intervals, the log-rank test p-values and the patients at risk. G Comparative depiction of the radiosensitizing effect upon target inhibition in MDA-MB-231 cells and the reduced OS in TNBC patients with target high expression. The inhibitor effect is presented as the 6 Gy sensitizing enhancement ratio (SER), and the effect on patient OS is represented as the -Log 10 (p-value) of the difference in patient OS between low and high expression. H Kaplan-Meier analyses using the METABRIC-TNBC patient cohort to assess the impact of radiotherapy (RT) on high and low PKM expression levels, with confidence intervals plotted, log-rank test p-values and patients at risk

Journal: Cell Communication and Signaling : CCS

Article Title: Precise metabolomics identifies glycolysis-related pyruvate kinase M activity as regulator of the S-phase-specific radiation response in triple-negative breast cancer cells

doi: 10.1186/s12964-026-02803-5

Figure Lengend Snippet: Identification of PKM as the most promising target for radiosensitization in TNBC cells. A Workflow illustrating the discovery of druggable candidates by database gene filtering on radiation-induced metabolic alterations. Image created with BioRender.com. B Venn diagram depicting the selection of metabolite-interacting genes through database alignment. C Gene filtering for the selection of potential therapeutic targets based on the indicated criteria. D Clonogenic basal survival (0 Gy) or clonogenic radiation survival (6 Gy) of MDA-MB-231 cells depleted of indicated candidates. Data are presented as enhancement ratios relative to non-specific siRNA controls, represented as mean ( n = 4), and colored based on significance (p-value) calculated by one-way ANOVA. E Combination of the target-specific inhibitors (IC 50 ) with irradiation (IR) in MDA-MB-231 cells ( n = 3). Results show mean ± SEM. Statistical significance was determined by unpaired two-tailed Student’s t-test and indicated as * p < 0.05; ** p < 0.01, or ns = not significant. F Kaplan-Meier analyses based on the mRNA expression of the indicated candidate genes using the METABRIC-TNBC patient cohort. 10-year overall survival (OS) curves show the highest vs. the lowest mRNA expression quartiles, the confidence intervals, the log-rank test p-values and the patients at risk. G Comparative depiction of the radiosensitizing effect upon target inhibition in MDA-MB-231 cells and the reduced OS in TNBC patients with target high expression. The inhibitor effect is presented as the 6 Gy sensitizing enhancement ratio (SER), and the effect on patient OS is represented as the -Log 10 (p-value) of the difference in patient OS between low and high expression. H Kaplan-Meier analyses using the METABRIC-TNBC patient cohort to assess the impact of radiotherapy (RT) on high and low PKM expression levels, with confidence intervals plotted, log-rank test p-values and patients at risk

Techniques: Selection, Biomarker Discovery, Irradiation, Two Tailed Test, Expressing, Inhibition

PKM inhibition compromises TNBC cell clonogenicity, viability and proliferation. A Workflow of functional analyses upon PKM targeting in combination with irradiation in TNBC cell models. Image created with BioRender.com. B Analysis of PKM mRNA expression in TNBC cells using the CCLE dataset. C Western blotting and densitometry from whole TNBC cell lysates to evaluate PKM levels in the indicated models (β-actin served as loading control). Protein levels were quantified using ImageJ software. D Clonogenic survival in irradiated Cal-51 and Cal-85-1 cells pretreated with IC 50 of PKM inhibitor compound 3 K. E Correlation of PKM expression levels with enhancement ratio after 4 Gy irradiation in indicated cell models. F Cell viability measured by CellTiterGlo in non-irradiated (0 Gy) or irradiated (6 Gy) PKM-depleted TNBC cells. G Proliferation of MDA-MB-231 cells based on cell number counted from day one to seven after indicated treatments. H Quantification of EdU-positive cells relative to total cell count. At least 100 cells were counted in each biological replicate and condition. I Representative immunofluorescence images of EdU-positive cells with J associated quantification of the corrected total cell fluorescence (at least 100 cells per biological replicate). Mean values of three independent experiments ± SD or SEM are shown. Statistical significance was determined by unpaired two-tailed Student’s t-test and indicated as: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; or ns not significant

Journal: Cell Communication and Signaling : CCS

Article Title: Precise metabolomics identifies glycolysis-related pyruvate kinase M activity as regulator of the S-phase-specific radiation response in triple-negative breast cancer cells

doi: 10.1186/s12964-026-02803-5

Figure Lengend Snippet: PKM inhibition compromises TNBC cell clonogenicity, viability and proliferation. A Workflow of functional analyses upon PKM targeting in combination with irradiation in TNBC cell models. Image created with BioRender.com. B Analysis of PKM mRNA expression in TNBC cells using the CCLE dataset. C Western blotting and densitometry from whole TNBC cell lysates to evaluate PKM levels in the indicated models (β-actin served as loading control). Protein levels were quantified using ImageJ software. D Clonogenic survival in irradiated Cal-51 and Cal-85-1 cells pretreated with IC 50 of PKM inhibitor compound 3 K. E Correlation of PKM expression levels with enhancement ratio after 4 Gy irradiation in indicated cell models. F Cell viability measured by CellTiterGlo in non-irradiated (0 Gy) or irradiated (6 Gy) PKM-depleted TNBC cells. G Proliferation of MDA-MB-231 cells based on cell number counted from day one to seven after indicated treatments. H Quantification of EdU-positive cells relative to total cell count. At least 100 cells were counted in each biological replicate and condition. I Representative immunofluorescence images of EdU-positive cells with J associated quantification of the corrected total cell fluorescence (at least 100 cells per biological replicate). Mean values of three independent experiments ± SD or SEM are shown. Statistical significance was determined by unpaired two-tailed Student’s t-test and indicated as: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; or ns not significant

Techniques: Inhibition, Functional Assay, Irradiation, Expressing, Western Blot, Control, Software, Cell Characterization, Immunofluorescence, Fluorescence, Two Tailed Test

PKM inhibition modulates DNA damage repair, DNA replication, and induces cell cycle arrest in irradiated TNBC cells. A Representative immunofluorescence images displaying RAD51 (green) and γH2AX (red) co-stained foci upon indicated treatment. Nuclei stained with DAPI (40× magnification). B Separated quantification of RAD51 and γH2AX foci using the Aklides ® NUK system (40×magnification). At least 100 cells were analyzed in each biological replicate. C Representative immunofluorescence images of pan-nuclear γH2AX staining with D associated manual quantification from Aklides images. E Determination of RAD51/γH2AX colocalization using the Aklides ® NUK system after indicated treatment. F Quantification of RAD51 foci per EdU-negative or -positive cell. G Cell cycle profiles with corresponding H quantification of MDA-MB-231 cells measured by flow cytometry upon propidium iodide staining. I Correlation of G2 phase cells (FACS analysis) with pan-nuclear γH2AX signal or colocalization of RAD51/γH2AX foci with corresponding Pearson coefficient (r) and p-value. J Treatment scheme for DNA fiber assay with representative immunofluorescence images for each treatment. K Total tract length of DNA fiber measured with ImageJ. At least 100 fibers were measured per biological replicate. L Tract length of each individual label of the DNA fiber. M Ratio of IdU and CldU tract length. Mean values of three independent experiments ± SD or SEM are shown. Statistical significance was determined by unpaired two-tailed Student’s t-test and indicated as: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; or ns not significant

Journal: Cell Communication and Signaling : CCS

Article Title: Precise metabolomics identifies glycolysis-related pyruvate kinase M activity as regulator of the S-phase-specific radiation response in triple-negative breast cancer cells

doi: 10.1186/s12964-026-02803-5

Figure Lengend Snippet: PKM inhibition modulates DNA damage repair, DNA replication, and induces cell cycle arrest in irradiated TNBC cells. A Representative immunofluorescence images displaying RAD51 (green) and γH2AX (red) co-stained foci upon indicated treatment. Nuclei stained with DAPI (40× magnification). B Separated quantification of RAD51 and γH2AX foci using the Aklides ® NUK system (40×magnification). At least 100 cells were analyzed in each biological replicate. C Representative immunofluorescence images of pan-nuclear γH2AX staining with D associated manual quantification from Aklides images. E Determination of RAD51/γH2AX colocalization using the Aklides ® NUK system after indicated treatment. F Quantification of RAD51 foci per EdU-negative or -positive cell. G Cell cycle profiles with corresponding H quantification of MDA-MB-231 cells measured by flow cytometry upon propidium iodide staining. I Correlation of G2 phase cells (FACS analysis) with pan-nuclear γH2AX signal or colocalization of RAD51/γH2AX foci with corresponding Pearson coefficient (r) and p-value. J Treatment scheme for DNA fiber assay with representative immunofluorescence images for each treatment. K Total tract length of DNA fiber measured with ImageJ. At least 100 fibers were measured per biological replicate. L Tract length of each individual label of the DNA fiber. M Ratio of IdU and CldU tract length. Mean values of three independent experiments ± SD or SEM are shown. Statistical significance was determined by unpaired two-tailed Student’s t-test and indicated as: * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; or ns not significant

Techniques: Inhibition, Irradiation, Immunofluorescence, Staining, Flow Cytometry, Two Tailed Test

$Glycolysis and TCA cycle enzymes share PKM effects on TNBC cell survival and radiation response. A Workflow of glycolysis and TCA cycle enzyme evaluation for a shared effect with PKM. Image created with BioRender.com. B Metabolite-gene interaction network of metabolites enriched upon PKM depletion and irradiation generated in MetaboAnalyst.ca. C Gene expression correlation between PKM and the selected enzymes in METABRIC-TNBC patient cohort. PKM significantly positively correlated genes are labelled. Pearson coefficients and p-values were calculated using Python. D Alignment of gene expression in METABRIC-TNBC patient cohort and the studied cell models from Cancer Cell Line Encyclopedia (CCLE). Heatmap was created with R, and data were hierarchically clustered (Ward.2) in rows based on patient gene expression, and in columns based on each heatmap samples. E Correlation analysis of gene expression between PKM and the labelled genes in ‘Fig. 6A’ in TNBC cell models. Data was obtained from CCLE, and Pearson coefficients and p-values were calculated using Prism. F Plating efficiencies and survival fractions of MDA-MB-231 cells upon single or PKM-double knockdown of the indicated enzymes. Normalized values (to control; n ≥ 3) are presented as mean ± SD and analyzed using one-way ANOVA and indicated as: * p < 0.05; ** p < 0.01. Single and double knockdown shared effects (within the PKM area) with a coefficient of variance (CV) lower than 35% are overlapped for 0 and 4 Gy X-ray irradiation. G Kaplan-Meier analysis based on the co-expression of cluster 1 from ‘Fig. 6F’ using the METABRIC-TNBC patient cohort. OS curves plot the highest vs. the lowest mRNA expression, confidence intervals, log-rank test p-values and patients at risk. H Kaplan-Meier analyses using the METABRIC-TNBC patient cohort to assess the impact of RT on high and low cluster 2 expression levels, confidence intervals, log-rank test p-values and patients at risk are plotted$

Journal: Cell Communication and Signaling : CCS

Article Title: Precise metabolomics identifies glycolysis-related pyruvate kinase M activity as regulator of the S-phase-specific radiation response in triple-negative breast cancer cells

doi: 10.1186/s12964-026-02803-5

Figure Lengend Snippet: Glycolysis and TCA cycle enzymes share PKM effects on TNBC cell survival and radiation response. A Workflow of glycolysis and TCA cycle enzyme evaluation for a shared effect with PKM. Image created with BioRender.com. B Metabolite-gene interaction network of metabolites enriched upon PKM depletion and irradiation generated in MetaboAnalyst.ca. C Gene expression correlation between PKM and the selected enzymes in METABRIC-TNBC patient cohort. PKM significantly positively correlated genes are labelled. Pearson coefficients and p-values were calculated using Python. D Alignment of gene expression in METABRIC-TNBC patient cohort and the studied cell models from Cancer Cell Line Encyclopedia (CCLE). Heatmap was created with R, and data were hierarchically clustered (Ward.2) in rows based on patient gene expression, and in columns based on each heatmap samples. E Correlation analysis of gene expression between PKM and the labelled genes in ‘Fig. 6A’ in TNBC cell models. Data was obtained from CCLE, and Pearson coefficients and p-values were calculated using Prism. F Plating efficiencies and survival fractions of MDA-MB-231 cells upon single or PKM-double knockdown of the indicated enzymes. Normalized values (to control; n ≥ 3) are presented as mean ± SD and analyzed using one-way ANOVA and indicated as: * p < 0.05; ** p < 0.01. Single and double knockdown shared effects (within the PKM area) with a coefficient of variance (CV) lower than 35% are overlapped for 0 and 4 Gy X-ray irradiation. G Kaplan-Meier analysis based on the co-expression of cluster 1 from ‘Fig. 6F’ using the METABRIC-TNBC patient cohort. OS curves plot the highest vs. the lowest mRNA expression, confidence intervals, log-rank test p-values and patients at risk. H Kaplan-Meier analyses using the METABRIC-TNBC patient cohort to assess the impact of RT on high and low cluster 2 expression levels, confidence intervals, log-rank test p-values and patients at risk are plotted

Techniques: Irradiation, Generated, Gene Expression, Knockdown, Control, Expressing

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