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ATCC mda mb 436
Mda Mb 436, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1173 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mda+mb+436/MDA-MB-436/10__1038_slash_s41523___026___01016___w-229-1-10
Average 97 stars, based on 1173 article reviews

mda mb 436 - by Bioz Stars, 2026-10

97/100 stars

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Multiple Displacement Amplification:

Article Title: Toxicarioside H induces cytoprotective autophagy by hindering the progression of necroptosis in triple-negative breast cancer cells
Article Snippet: Additionally, we acquired a CF488-conjugated goat anti-mouse IgG antibody (SAB4600388) from Sigma-Aldrich (St. Louis, MO, USA). .. 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. ..

Article Title: Nitroalkenes Exploit Dependence on Autophagy-Lysosome Pathway in PARPi-Resistant Triple Negative Breast Cancer.
Article Snippet: This is a PDF of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability.. This version will undergo additional copyediting, typesetting and review before it is published in its final form.. As such, this version is no longer the Accepted Manuscript, but it is not yet the definitive Version of Record; we are providing this early version to give early visibility of the article.

Article Title: CXCL12/ZNF503/GATA3/MMP1 axis promotes tumor progression and metastasis of triple-negative breast cancer
Article Snippet: .. The human triple-negative breast cancer cell lines, MDA-MB-231 (MM231), BT-549, MDA-MB-436 (MM436), MDA-MB-435 S (MM435S) and the non-triple-negative breast cancer (non-TNBC) cell line MCF-7 were obtained from American Type Culture Collection (ATCC, USA). .. Lentiviral particles carrying specific short hairpin RNAs (shRNAs) were used to achieve gene knockdown (GeneChem, Shanghai, China; Table ).

Article Title: Polyphyllin VI induces Forkhead box O3 nuclear liquid-liquid phase separation to promote mitophagy in breast cancer.
Article Snippet: Background: Mitochondrial dysfunction and defective mitophagy are closely associated with cancer progression.. Forkhead box O3 (FOXO3), a key transcription factor, promotes autophagy by activating autophagy-related genes.. Polyphyllin VI (PPVI), a Paris polyphylla-derived steroidal saponin, displays potent antitumor activity.

Article Title: Targeting SIK2 with GRN-300 Potentiates Paclitaxel Efficacy in Triple-Negative Breast Cancer.
Article Snippet: .. Human breast cancer cell lines (MDA-MB-231 (MB-231), MDA-MB-436 (MB-436), MDA-MB-468 (MB-468), MDA-MB-453 (MB-453), SUM159, HCC1143, HCC1395, HCC1428, HCC1569, HCC1937, HCC1954, HCC202, HCC38, HCC70, BT-474, T47D, MCF7, SKBr3, and ZR75-1) were obtained from ATCC (Manassas, VA, USA) and Cal51 was purchased from Creative Bioarray (Shirley, NY, USA). ..

Article Title: Cell-free detection of methylated prostate tumour
Article Snippet: .. Tests for Other Subtypes A number of breast cell lines from women with known BRCA1 mutations have been isolated such as MDA-MB-436, HCC1937 and HCC1395 (all available from ATCC). ..

Article Title: “Molecular divergence shapes lung- and liver-preferential metastasis in HER2-positive breast cancer”
Article Snippet: .. MDA-MB-231, MDA-MB-436, and MCF7 cell lines were purchased from the American Type Culture Collection (ATCC, Rockville, MD). .. All NT2.5-based cell lines were cultured in RPMI supplemented with 20% fetal bovine serum (FBS; Gibco), 100 U/mL penicillin, 100 U/mL streptomycin, 0.1% nonessential amino acids, 0.1% glutamine and 10mM N-2hydroxyethylpiperazine-N-2-ethane sulfonic acid (HEPES; STEMCELL Technologies, Vancouver, Canada) at 37°C in a humidified 5% CO2 incubator.

Cell Culture:

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other:

Article Title: Squamous-state excursions activate APOBEC3A in cancer
Article Snippet: For pan-cell line analysis of APOBEC3A and APOBEC3B expression, AU565, BT20,BT-474, Cama1, DU4475, HCC1395, HCC1428, HCC1500, HCC1599, HCC1806, HCC1937, HCC1954, HCC202, HCC2157, HCC2218, HCC38, HCC70, Hs578T, MCF10A, MCF10F, MCF12A, MCF7, MDA-MB-157, MDA-MB-175-VII, MDA-MB-231, MDA-MB-361, MDA-MB-415, MDA-MB-436, MDA-MB-453, MDA-MB-468, SKBR3, T47D, UACC893, and Zr-75-30 cells were obtained from ATCC and cultured according to ATCC recommendations.

Isolation:

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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.

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.

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

A) Experimental scheme for the selection of saruparib-resistant cell lines derived from MDA-MB-436 cells. B) Comparison of cell morphology of MDA-MB-436 and SR cell lines. C) Normalized confluence over time for MDA-MB-436 and SR cells as measured by Incucyte live-cell imaging. D) Dose-response curves for MDA-MB-436 and SR cells treated with saruparib. E) SR cell lines’ fold-changes in saruparib IC50 values relative to parental MDA-MB-436 cells derived from the data in panel D. F) Assessment of tumor growth of MDA-MB-436 cells and G) 436-SR-1 cells subcutaneously implanted in NSG mice. Mice were treated via oral gavage with doses indicated by the solid bars. Data in panels C, D, F, and G are depicted as mean ± SEM.

Journal: bioRxiv

Article Title: PARP1 catalytic domain mutations drive high-level resistance to saruparib while preserving DNA damage response vulnerabilities

doi: 10.64898/2026.05.08.723870

Figure Lengend Snippet: A) Experimental scheme for the selection of saruparib-resistant cell lines derived from MDA-MB-436 cells. B) Comparison of cell morphology of MDA-MB-436 and SR cell lines. C) Normalized confluence over time for MDA-MB-436 and SR cells as measured by Incucyte live-cell imaging. D) Dose-response curves for MDA-MB-436 and SR cells treated with saruparib. E) SR cell lines’ fold-changes in saruparib IC50 values relative to parental MDA-MB-436 cells derived from the data in panel D. F) Assessment of tumor growth of MDA-MB-436 cells and G) 436-SR-1 cells subcutaneously implanted in NSG mice. Mice were treated via oral gavage with doses indicated by the solid bars. Data in panels C, D, F, and G are depicted as mean ± SEM.

Article Snippet: MDA-MB-436 cells (ATCC) were cultured in 1:1 DMEM:Ham’s F12 medium (Corning) supplemented with 10% FBS and penicillin/streptomycin.

Techniques: Selection, Derivative Assay, Comparison, Live Cell Imaging

Dose-response curves for MDA-MB-436 and SR cells treated with A) olaparib, B) talazoparib, C) niraparib, or D) stenoparib. E) SR cell lines’ fold-changes in olaparib, talazoparib, niraparib, and stenoparib IC50 values relative to parental MDA-MB-436 cells derived from the data in panels A-D. F) Measurement of homologous recombination activity using an extrachromosomal reporter assay. BRCA1-proficient MDA-MB-468 cells were used as a positive control. Data in panels A-D and F are depicted as mean ± SEM from triplicate experiments. **** P < 0.0001.

Journal: bioRxiv

Article Title: PARP1 catalytic domain mutations drive high-level resistance to saruparib while preserving DNA damage response vulnerabilities

doi: 10.64898/2026.05.08.723870

Figure Lengend Snippet: Dose-response curves for MDA-MB-436 and SR cells treated with A) olaparib, B) talazoparib, C) niraparib, or D) stenoparib. E) SR cell lines’ fold-changes in olaparib, talazoparib, niraparib, and stenoparib IC50 values relative to parental MDA-MB-436 cells derived from the data in panels A-D. F) Measurement of homologous recombination activity using an extrachromosomal reporter assay. BRCA1-proficient MDA-MB-468 cells were used as a positive control. Data in panels A-D and F are depicted as mean ± SEM from triplicate experiments. **** P < 0.0001.

Article Snippet: MDA-MB-436 cells (ATCC) were cultured in 1:1 DMEM:Ham’s F12 medium (Corning) supplemented with 10% FBS and penicillin/streptomycin.

Techniques: Derivative Assay, Homologous Recombination, Activity Assay, Reporter Assay, Positive Control

$A) Representative Western blots of PARP1 and PARP2 expression and MAR/PARylation from the soluble fraction of MDA-MB-436 and SR cells in response to 0.1 mg/mL MMS treatment for 2 hours. Representative Western blots of soluble and chromatin-bound fractions from B) MDA-MB-436, C) 436-SR-1, D) 436-SR-4, E) 436-SR-5, F) 436-SR-9, and G) 436-SR-10 cells treated with DMSO control, 0.1 mg/mL MMS, and/or 0.2, 2, 20, 200 nM saruparib for 2 hours. H) Quantification of saruparib inhibition of MAR/PARylation in MDA-MB-436 and SR cells from panels B-G. I) Quantification of saruparib-induced PARP1 trapping in MDA-MB-436 and SR cells from panels B-G.$

Journal: bioRxiv

Article Title: PARP1 catalytic domain mutations drive high-level resistance to saruparib while preserving DNA damage response vulnerabilities

doi: 10.64898/2026.05.08.723870

Figure Lengend Snippet: A) Representative Western blots of PARP1 and PARP2 expression and MAR/PARylation from the soluble fraction of MDA-MB-436 and SR cells in response to 0.1 mg/mL MMS treatment for 2 hours. Representative Western blots of soluble and chromatin-bound fractions from B) MDA-MB-436, C) 436-SR-1, D) 436-SR-4, E) 436-SR-5, F) 436-SR-9, and G) 436-SR-10 cells treated with DMSO control, 0.1 mg/mL MMS, and/or 0.2, 2, 20, 200 nM saruparib for 2 hours. H) Quantification of saruparib inhibition of MAR/PARylation in MDA-MB-436 and SR cells from panels B-G. I) Quantification of saruparib-induced PARP1 trapping in MDA-MB-436 and SR cells from panels B-G.

Article Snippet: MDA-MB-436 cells (ATCC) were cultured in 1:1 DMEM:Ham’s F12 medium (Corning) supplemented with 10% FBS and penicillin/streptomycin.

Techniques: Western Blot, Expressing, Control, Inhibition

Dose-response curves for MDA-MB-436 and SR cells treated with A) cisplatin, B) camptothecin (CPT), C) paclitaxel, D) ceralasertib, E) MK-1775, and F) NERx-329. All data are depicted as mean ± SEM from triplicate experiments.

Journal: bioRxiv

Article Title: PARP1 catalytic domain mutations drive high-level resistance to saruparib while preserving DNA damage response vulnerabilities

doi: 10.64898/2026.05.08.723870

Figure Lengend Snippet: Dose-response curves for MDA-MB-436 and SR cells treated with A) cisplatin, B) camptothecin (CPT), C) paclitaxel, D) ceralasertib, E) MK-1775, and F) NERx-329. All data are depicted as mean ± SEM from triplicate experiments.

Article Snippet: MDA-MB-436 cells (ATCC) were cultured in 1:1 DMEM:Ham’s F12 medium (Corning) supplemented with 10% FBS and penicillin/streptomycin.

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