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tnbc cell lines  (ATCC)


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    Structured Review

    ATCC tnbc cell lines
    Effects of ToxH on <t>TNBC</t> cell proliferation and cell death. <t>TNBC</t> <t>MDA-MB-231,</t> MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.
    Tnbc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1131 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    tnbc cell lines - by Bioz Stars, 2026-05
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    Images

    1) Product Images from "Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells"

    Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

    Journal: Translational Oncology

    doi: 10.1016/j.tranon.2026.102779

    Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.
    Figure Legend Snippet: Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Techniques Used: CCK-8 Assay, Control, EdU Assay, Fluorescence, Flow Cytometry, Staining

    ToxH triggers the complete autophagic process in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 cells were treated with or without ToxH for 24 h and transfected with or without the corresponding plasmid. (A) Western blotting detection shows an increase in the expression of LC3-II, ATG5, and Beclin-1, but a decrease in the expression of p62. (B) Immunofluorescence observation reveals that ToxH treatment generated a considerable number of LC3B puncta. (C) TNBC cells transfected with the mCherry-GFP-LC3 plasmid demonstrate an observable increase in the formation of autophagosomes (yellow puncta) and autolysosomes (red puncta) that were treated with ToxH. Data are presented as mean ± SD and analyzed using an Unpaired t-test (A) or two-way ANOVA with Tukey's multiple comparisons test (B and C), N = 3 (A) or 100 (B and C); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.
    Figure Legend Snippet: ToxH triggers the complete autophagic process in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 cells were treated with or without ToxH for 24 h and transfected with or without the corresponding plasmid. (A) Western blotting detection shows an increase in the expression of LC3-II, ATG5, and Beclin-1, but a decrease in the expression of p62. (B) Immunofluorescence observation reveals that ToxH treatment generated a considerable number of LC3B puncta. (C) TNBC cells transfected with the mCherry-GFP-LC3 plasmid demonstrate an observable increase in the formation of autophagosomes (yellow puncta) and autolysosomes (red puncta) that were treated with ToxH. Data are presented as mean ± SD and analyzed using an Unpaired t-test (A) or two-way ANOVA with Tukey's multiple comparisons test (B and C), N = 3 (A) or 100 (B and C); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Techniques Used: Transfection, Plasmid Preparation, Western Blot, Expressing, Immunofluorescence, Generated

    Combination of ToxH and CQ treatments increases anti-tumor activity through promotion of necroptosis in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 tumor models were established in female nude mice and treated with ToxH or combined with CQ for five mice in each group. (A) Tumor images were captured at day 18 after tumor cell inoculation. (B) Tumor volumes were measured at day 18 after the tumor cell inoculation. (C) Western blotting detection of the autophagy marker proteins LC3 and p62, and necroptosis marker proteins RIPK1, RIPK3, and MLKL and phosphorylated MLKL (pMLKL) in the tumor tissues treated with the indicated reagents. (D) Immunohistochemical detection of the necroptosis marker phosphorylated proteins pRIPK3 and pMLKL. Data are presented as mean ± SD and were assessed using one-way ANOVA with Tukey's post hoc test, where N = 5 (A and B) or representative images from triplicate experiments (C and D); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, no significant.
    Figure Legend Snippet: Combination of ToxH and CQ treatments increases anti-tumor activity through promotion of necroptosis in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 tumor models were established in female nude mice and treated with ToxH or combined with CQ for five mice in each group. (A) Tumor images were captured at day 18 after tumor cell inoculation. (B) Tumor volumes were measured at day 18 after the tumor cell inoculation. (C) Western blotting detection of the autophagy marker proteins LC3 and p62, and necroptosis marker proteins RIPK1, RIPK3, and MLKL and phosphorylated MLKL (pMLKL) in the tumor tissues treated with the indicated reagents. (D) Immunohistochemical detection of the necroptosis marker phosphorylated proteins pRIPK3 and pMLKL. Data are presented as mean ± SD and were assessed using one-way ANOVA with Tukey's post hoc test, where N = 5 (A and B) or representative images from triplicate experiments (C and D); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, no significant.

    Techniques Used: Activity Assay, Western Blot, Marker, Immunohistochemical staining



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    Image Search Results


    Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Journal: Translational Oncology

    Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

    doi: 10.1016/j.tranon.2026.102779

    Figure Lengend Snippet: Effects of ToxH on TNBC cell proliferation and cell death. TNBC MDA-MB-231, MDA-MB-468, and HCC 38 cells were treated with different concentrations of ToxH as indicated for 24 h. (A) Cell viability was assessed using the CCK-8 assay, represented as a percentage relative to the control group (Ctrl). (B) Representative images from the EdU assay showing proliferating cells (red fluorescence). (C) Quantification of EdU-positive proliferating cells by flow cytometry, represented as a percentage relative to the control group (Ctrl). (D) Representative flow cytometry images showing the intensity of 7-AAD-stained cells. (E) Percentage of 7-AAD-positive dead cells determined by flow cytometry. (F) Measurement of LDH release, represented as fold change relative to the control group (Ctrl). Data are presented as mean ± SD and analyzed using one-way ANOVA with Tukey's multiple comparisons test, N = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Article Snippet: The TNBC cell lines used in this study, including MDA-MB-231, MDA-MB-436, and HCC 38, were obtained from the American Type Culture Collection (ATCC) and maintained in our laboratory.

    Techniques: CCK-8 Assay, Control, EdU Assay, Fluorescence, Flow Cytometry, Staining

    ToxH triggers the complete autophagic process in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 cells were treated with or without ToxH for 24 h and transfected with or without the corresponding plasmid. (A) Western blotting detection shows an increase in the expression of LC3-II, ATG5, and Beclin-1, but a decrease in the expression of p62. (B) Immunofluorescence observation reveals that ToxH treatment generated a considerable number of LC3B puncta. (C) TNBC cells transfected with the mCherry-GFP-LC3 plasmid demonstrate an observable increase in the formation of autophagosomes (yellow puncta) and autolysosomes (red puncta) that were treated with ToxH. Data are presented as mean ± SD and analyzed using an Unpaired t-test (A) or two-way ANOVA with Tukey's multiple comparisons test (B and C), N = 3 (A) or 100 (B and C); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Journal: Translational Oncology

    Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

    doi: 10.1016/j.tranon.2026.102779

    Figure Lengend Snippet: ToxH triggers the complete autophagic process in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 cells were treated with or without ToxH for 24 h and transfected with or without the corresponding plasmid. (A) Western blotting detection shows an increase in the expression of LC3-II, ATG5, and Beclin-1, but a decrease in the expression of p62. (B) Immunofluorescence observation reveals that ToxH treatment generated a considerable number of LC3B puncta. (C) TNBC cells transfected with the mCherry-GFP-LC3 plasmid demonstrate an observable increase in the formation of autophagosomes (yellow puncta) and autolysosomes (red puncta) that were treated with ToxH. Data are presented as mean ± SD and analyzed using an Unpaired t-test (A) or two-way ANOVA with Tukey's multiple comparisons test (B and C), N = 3 (A) or 100 (B and C); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, not significant.

    Article Snippet: The TNBC cell lines used in this study, including MDA-MB-231, MDA-MB-436, and HCC 38, were obtained from the American Type Culture Collection (ATCC) and maintained in our laboratory.

    Techniques: Transfection, Plasmid Preparation, Western Blot, Expressing, Immunofluorescence, Generated

    Combination of ToxH and CQ treatments increases anti-tumor activity through promotion of necroptosis in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 tumor models were established in female nude mice and treated with ToxH or combined with CQ for five mice in each group. (A) Tumor images were captured at day 18 after tumor cell inoculation. (B) Tumor volumes were measured at day 18 after the tumor cell inoculation. (C) Western blotting detection of the autophagy marker proteins LC3 and p62, and necroptosis marker proteins RIPK1, RIPK3, and MLKL and phosphorylated MLKL (pMLKL) in the tumor tissues treated with the indicated reagents. (D) Immunohistochemical detection of the necroptosis marker phosphorylated proteins pRIPK3 and pMLKL. Data are presented as mean ± SD and were assessed using one-way ANOVA with Tukey's post hoc test, where N = 5 (A and B) or representative images from triplicate experiments (C and D); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, no significant.

    Journal: Translational Oncology

    Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells

    doi: 10.1016/j.tranon.2026.102779

    Figure Lengend Snippet: Combination of ToxH and CQ treatments increases anti-tumor activity through promotion of necroptosis in TNBC cells. MDA-MB-231, MDA-MB-438, and HHC-38 tumor models were established in female nude mice and treated with ToxH or combined with CQ for five mice in each group. (A) Tumor images were captured at day 18 after tumor cell inoculation. (B) Tumor volumes were measured at day 18 after the tumor cell inoculation. (C) Western blotting detection of the autophagy marker proteins LC3 and p62, and necroptosis marker proteins RIPK1, RIPK3, and MLKL and phosphorylated MLKL (pMLKL) in the tumor tissues treated with the indicated reagents. (D) Immunohistochemical detection of the necroptosis marker phosphorylated proteins pRIPK3 and pMLKL. Data are presented as mean ± SD and were assessed using one-way ANOVA with Tukey's post hoc test, where N = 5 (A and B) or representative images from triplicate experiments (C and D); * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001; ns, no significant.

    Article Snippet: The TNBC cell lines used in this study, including MDA-MB-231, MDA-MB-436, and HCC 38, were obtained from the American Type Culture Collection (ATCC) and maintained in our laboratory.

    Techniques: Activity Assay, Western Blot, Marker, Immunohistochemical staining

    Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on TNBC cell lines (MDA‐MB‐231 and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.

    Journal: Drug Development Research

    Article Title: Design, Synthesis, Biological Evaluation, and Molecular Modeling Studies of Novel 2‐Aminothiazole Derivatives as Potential FOXM1 Inhibitors for Triple‐Negative Breast Cancer Therapy and Structure‐Activity Relationship

    doi: 10.1002/ddr.70296

    Figure Lengend Snippet: Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on TNBC cell lines (MDA‐MB‐231 and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.

    Article Snippet: The human TNBC cell lines (BT‐549, BT‐20 and MDA‐MB‐231) from the American Type Culture Collection (ATCC, Manassas, VA, USA) were used.

    Techniques: Expressing, Control

    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

    ALDH activity in triple-negative breast cancer MDA-MB-231 and invasive ductal carcinoma-derived KAIMRC1 cells measurements using a colorimetric assay. KAIMRC1 stem-like cells showed higher ALDH activity when compared with that of MDA-MB-231 cells. Data are presented as the mean ± SD from three independent experiments. Statistical significance relative to MDA-MB-231 cells is indicated as *P<0.05. ALDH, aldehyde dehydrogenase.

    Journal: Oncology Letters

    Article Title: Methylglyoxal-derived glycated albumin enhances the stemness potential of invasive ductal carcinoma-derived breast cancer stem-like cell line KAIMRC1

    doi: 10.3892/ol.2026.15541

    Figure Lengend Snippet: ALDH activity in triple-negative breast cancer MDA-MB-231 and invasive ductal carcinoma-derived KAIMRC1 cells measurements using a colorimetric assay. KAIMRC1 stem-like cells showed higher ALDH activity when compared with that of MDA-MB-231 cells. Data are presented as the mean ± SD from three independent experiments. Statistical significance relative to MDA-MB-231 cells is indicated as *P<0.05. ALDH, aldehyde dehydrogenase.

    Article Snippet: The TNBC cell line MDA-MB-231 (cat. no. HTB-26, American Type Culture Collection) was maintained in complete DMEM supplemented with the aforementioned components.

    Techniques: Activity Assay, Derivative Assay, Colorimetric Assay