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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:
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:
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:
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:
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:
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:
Techniques: Expressing, Transfection, Negative Control, Western Blot, Software, Incubation, Control, Fluorescence, Epifluorescence Microscopy
Journal: Biomolecules & Therapeutics
Article Title: Zoledronic Acid Inhibits the Growth of ER-Positive Breast Cancer Cells by Inducing Ferroptosis
doi: 10.4062/biomolther.2025.132
Figure Lengend Snippet: Zoledronic Acid Induces Ferroptosis in ER+ Breast Cancer Cells. (A) Dose-dependent growth inhibition by zoledronic acid (ZA). MCF-7 and ZR-75-1 cells were treated with increasing ZA concentrations (0-80 μM) for 72 h, followed by CCK-8 viability assays. (B) Intracellular iron accumulation quantified by colorimetric assay. Cells exposed to 40 μM ZA for 24 h showed elevated iron levels. (C, D) ZA-induced lipid peroxidation in MCF-7 (C) and ZR-75-1 (D) was detected by flow cytometry. Cells treated with 40 μM ZA for 24 h exhibited increased BODIPY 581/591 C11 oxidation. ** p <0.01; *** p <0.001.
Article Snippet:
Techniques: Inhibition, CCK-8 Assay, Colorimetric Assay, Flow Cytometry
Journal: Biomolecules & Therapeutics
Article Title: Zoledronic Acid Inhibits the Growth of ER-Positive Breast Cancer Cells by Inducing Ferroptosis
doi: 10.4062/biomolther.2025.132
Figure Lengend Snippet: Ferrostatin-1 Attenuates ZA-Induced Ferroptosis. (A, B) Lipid ROS suppression by ferroptosis inhibition. Co-treatment with 5 μM Ferrostatin-1 (Ferro-1) partially reversed ZA-induced BODIPY 581/591 C11 oxidation in MCF-7 (A) and ZR-75-1 (B). (C) Viability rescue by Ferro-1. CCK-8 assays demonstrated partial recovery of cell growth in ZA (40 μM)+Ferro-1 (5 μM) co-treated groups after 48 h. * p <0.05; ** p <0.01; *** p <0.001.
Article Snippet:
Techniques: Inhibition, CCK-8 Assay
Journal: Biomolecules & Therapeutics
Article Title: Zoledronic Acid Inhibits the Growth of ER-Positive Breast Cancer Cells by Inducing Ferroptosis
doi: 10.4062/biomolther.2025.132
Figure Lengend Snippet: Synergistic Ferroptosis Induction by ZA and RSL3. (A, B) Enhanced lipid peroxidation with combination therapy. RSL3 (5 μM) potentiated ZA-induced BODIPY 581/591 C11 oxidation in MCF-7 (A) and ZR-75-1 (B). (C) Cooperative growth inhibition. Crystal violet colony formation assay demonstrated ZA (40 μM)+RSL3 (5 μM) co-treatment for 6 days showed enhanced cytotoxicity compared to single agents. * p <0.05; ** p <0.01; *** p <0.001.
Article Snippet:
Techniques: Inhibition, Colony Assay
Journal: Biomolecules & Therapeutics
Article Title: Zoledronic Acid Inhibits the Growth of ER-Positive Breast Cancer Cells by Inducing Ferroptosis
doi: 10.4062/biomolther.2025.132
Figure Lengend Snippet: ZA Downregulates Ferroptosis Suppressors SLC7A11 and GPX4. (A, B) Dose-dependent protein suppression. Western blot analysis revealed decreased SLC7A11 and GPX4 expression in MCF-7 (A) and ZR-75-1 (B) after 24 h ZA treatment (20-40 μM). Tubulin served as loading control.
Article Snippet:
Techniques: Western Blot, Expressing, Control
Journal: Biomolecules & Therapeutics
Article Title: Zoledronic Acid Inhibits the Growth of ER-Positive Breast Cancer Cells by Inducing Ferroptosis
doi: 10.4062/biomolther.2025.132
Figure Lengend Snippet: ZA Activates Hippo Signaling Through YAP Regulation. (A) Phospho-YAP induction and total YAP reduction. Dose-responsive YAP phosphorylation and protein degradation in cells treated with ZA (20-40 μM) for 24 h. (B, C) Transcriptional downregulation of YAP targets. qRT-PCR showed decreased CTGF (B) and CYR61 (C) mRNA levels post-ZA treatment. (D) Accelerated YAP protein turnover. Cycloheximide (10 μM) chase assay demonstrated enhanced YAP degradation kinetics in MCF-7 cells pre-treated with 40 μM ZA. (E) YAP nuclear export. Immunofluorescence revealed dose-dependent reduction of nuclear YAP (green) in ZA-treated MCF-7 cells (8 h). Hoechst (blue) marks nuclei. Scale bar: 20 μm. ** p <0.01; *** p <0.001; ns: no significance.
Article Snippet:
Techniques: Phospho-proteomics, Quantitative RT-PCR, Immunofluorescence