mda-mb-468  (ATCC)

Journal: Translational Oncology

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

doi: 10.1016/j.tranon.2026.102777

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

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

Techniques: Expressing, Transformation Assay, Western Blot, Software

Journal: Translational Oncology

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

doi: 10.1016/j.tranon.2026.102777

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

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

Techniques: Concentration Assay

Journal: Translational Oncology

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

doi: 10.1016/j.tranon.2026.102777

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

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

Techniques: Expressing, Western Blot, Software

Journal: Translational Oncology

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

doi: 10.1016/j.tranon.2026.102777

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

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

Techniques: Control, Imaging, Concentration Assay

Journal: Translational Oncology

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

doi: 10.1016/j.tranon.2026.102777

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

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

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

Journal: Translational Oncology

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

doi: 10.1016/j.tranon.2026.102777

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

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

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

Journal: Journal of Molecular Medicine (Berlin, Germany)

Article Title: MEK inhibitor cobimetinib increases calreticulin and induces immune modulation in TNBC

doi: 10.1007/s00109-026-02684-8

Figure Lengend Snippet: Cobimetinib induces cell apoptosis and upregulates DAMPs in murine TNBC cells. (a–c) 4T1 cells were exposed to varying concentrations of cobimetinib for MTT assays ( a ), flow cytometry analysis ( b ), and ATP measurements ( c ). ( d ) Whole-cell extracts from 4T1 cells treated with cobimetinib or the vehicle were subjected to Western blot analysis. ( e ) Western blot analysis assessed the cytoplasmic and membrane fractions of cells. ( f ) Flow cytometry analysis was employed to examine the surface expression of CRT. Student’s t -test, * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: Human TNBC cell lines (MDA-MB-231 and MDA-MB-468) and a murine TNBC cell line (4T1) were obtained from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Flow Cytometry, Western Blot, Membrane, Expressing

Journal: Journal of Molecular Medicine (Berlin, Germany)

Article Title: MEK inhibitor cobimetinib increases calreticulin and induces immune modulation in TNBC

doi: 10.1007/s00109-026-02684-8

Figure Lengend Snippet: Cobimetinib treatment induces the expression of DAMPs and proapoptotic proteins in human TNBC cells. ( a ) MDA-MB-231 and MDA-MB-468 cells were exposed to cobimetinib at various concentrations for 3 days and evaluated for cell viability through MTT assay. ( b ) Flow cytometry analysis was conducted to assess apoptosis induction in cobimetinib-treated cells. ( c ) Flow cytometry analysis was used to detect surface CRT expression in 4T1 cells treated with cobimetinib or the vehicle. ( d ) Western blot analysis was performed on whole-cell extracts from cobimetinib- or vehicle-treated MDA-MB-231 and MDA-MB-468 cells to examine the expression of pro-apoptotic proteins. Student’s t -test, * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: Human TNBC cell lines (MDA-MB-231 and MDA-MB-468) and a murine TNBC cell line (4T1) were obtained from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Expressing, MTT Assay, Flow Cytometry, Western Blot

Journal: Journal of Molecular Medicine (Berlin, Germany)

Article Title: MEK inhibitor cobimetinib increases calreticulin and induces immune modulation in TNBC

doi: 10.1007/s00109-026-02684-8

Figure Lengend Snippet: Cobimetinib reduces TNBC tumor growth and induces ICD in vivo. ( a – g ) Nude mice and BALB/c mice with 4T1 tumors received treatment with cobimetinib at 10 mg/kg QD or the vehicle. Tumor sizes ( a and b ), tumor weights ( c and d ), mouse body weights ( e and f ), and survival rates ( g ) were measured. (h and i) Xenografted tumors from vehicle-treated mice (designated as D3, E4, F2, and F4) and cobimetinib-treated mice (designated as D4, E1, F1, and F5) were harvested and subjected to Western blot analysis ( h ) and immunohistochemical staining ( i ) using antibodies against pERK, ERK, CRT, HMGB1, and M30 CytoDEATH (CK18). Survival curves represent actual animal survival, not tumor size-based euthanasia; all BALB/c mice remained alive until day 22. Student’s t-test, * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bar, 100 μm

Article Snippet: Human TNBC cell lines (MDA-MB-231 and MDA-MB-468) and a murine TNBC cell line (4T1) were obtained from the American Type Culture Collection (Manassas, VA, USA).

Techniques: In Vivo, Western Blot, Immunohistochemical staining, Staining

Journal: Frontiers in Immunology

Article Title: An integrated analysis of SLC7A11 as a pan-cancer immunotherapeutic biomarker with experimental validation of its regulation by miR-148b-3p in breast cancer

doi: 10.3389/fimmu.2026.1752767

Figure Lengend Snippet: SLC7A11 promotes TNBC cell models progression and ferroptosis via regulation of miR-148b-3p. (A) Validation of miR-148b-3p knockdown efficiency by qRT-PCR, with U6 as an internal control. (B, C) Expression levels of SLC7A11 mRNA (B) and protein (C) were determined by qRT-PCR and western blotting, respectively, showing that miR-148b-3p inhibition significantly upregulated SLC7A11. GAPDH was used as the loading control. Uncropped western blot images are provided as Supplementary Figure 8 . (D) MiR-148b-3p inhibitors or control were transfected into MDA-MB-231 cells. Cell proliferation was measured using CCK-8 assay. (E) Transwell assay was used for cell migration of MDA-MB-231 cells. (F–H) The miR-148b-3p/SLC7A11 axis modulated erastin-induced ferroptosis. MDA-MB-231 or MDA-MB-468 cells were transfected with control or miR-148b-3p inhibitors for 24 hours, followed by SLC7A11 overexpression, and then treated with 10 μM erastin. The MDA level (F) , GSH level (G) , and cell viability (H) were determined in indicated cells. Data are presented as mean ± SD from three biological replicates. * indicates P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

Article Snippet: TNBC cell models MDA-MB-231 and MDA-MB-468 were obtained from the American Type Culture Collection (ATCC).

Techniques: Biomarker Discovery, Knockdown, Quantitative RT-PCR, Control, Expressing, Western Blot, Inhibition, Transfection, CCK-8 Assay, Transwell Assay, Migration, Over Expression