human breast cancer cell lines t47d  (ATCC)

Journal: Scientific Reports

Article Title: Development of a pH-responsive pegylated chitosan nanocarrier for targeted delivery of 17-AAG and synergistic therapy in HER2 + breast cancer

doi: 10.1038/s41598-025-30507-2

Figure Lengend Snippet: Synergistic cytotoxic effect of 17-AAG-loaded PEG-CS nanoparticles and trastuzumab on T47D cells. Cell viability was assessed by MTT assay after 72 h of treatment. Data are presented as mean ± SD ( n = 3). The combination group (17-AAG-loaded NPs + trastuzumab) showed significantly reduced cell viability (15%) compared to treatment with 17-AAG-loaded NPs alone (50%), trastuzumab alone (35%), or blank NPs + trastuzumab (100%). Statistical significance: **** p < 0.0001 vs. Blank NPs + Trastuzumab group (one-way ANOVA with Tukey’s post-hoc test). The Combination Index (CI) calculated using CompuSyn software was 0.72, indicating strong synergy.

Article Snippet: The T47D human breast cancer cell line was obtained from the Pasteur Institute of Iran.

Techniques: MTT Assay, Software

Journal: Scientific Reports

Article Title: Development of a pH-responsive pegylated chitosan nanocarrier for targeted delivery of 17-AAG and synergistic therapy in HER2 + breast cancer

doi: 10.1038/s41598-025-30507-2

Figure Lengend Snippet: In vitro cytotoxicity of 17-AAG-loaded PEG-CS NPs in T47D and MDA-MB-231 cells. Cell viability after 72 h treatment with free 17-AAG or 17-AAG-loaded NPs. The nanoformulation showed significantly enhanced cytotoxicity, with an IC₅₀ of 2.3 ± 0.3 µM in T47D cells, representing a threefold increase compared to free 17-AAG (IC₅₀ = 6.9 ± 0.5 µM). Similar results were observed in MDA-MB-231 cells (IC₅₀ = 3.0 µM for NPs vs. 8.1 µM for free drug). Blank PEG-CS NPs showed no significant toxicity in NHDF cells (up to 50 µg/mL). Data are mean ± SEM ( n = 3). Statistical significance was determined by one-way ANOVA followed by Tukey’s post-hoc test. **** P < 0.0001 vs. control.

Article Snippet: The T47D human breast cancer cell line was obtained from the Pasteur Institute of Iran.

Techniques: In Vitro, Control

Journal: Scientific Reports

Article Title: Development of a pH-responsive pegylated chitosan nanocarrier for targeted delivery of 17-AAG and synergistic therapy in HER2 + breast cancer

doi: 10.1038/s41598-025-30507-2

Figure Lengend Snippet: Flow cytometric analysis of apoptosis in T47D cells after 24 h treatment with 17-AAG-loaded PEG-CS NPs. A Untreated control cells. B Cells treated with 17-AAG-loaded PEG-CS NPs. The percentage of apoptotic cells (Q2 + Q3) increased from 16.5% in the control group to 52.2% in the treated group. Data are representative of three independent experiments ( n = 3).

Article Snippet: The T47D human breast cancer cell line was obtained from the Pasteur Institute of Iran.

Techniques: Control

Journal: Scientific Reports

Article Title: Development of a pH-responsive pegylated chitosan nanocarrier for targeted delivery of 17-AAG and synergistic therapy in HER2 + breast cancer

doi: 10.1038/s41598-025-30507-2

Figure Lengend Snippet: Cell cycle distribution in T47D cells after 24 h treatment with 17-AAG-loaded PEG-CS NPs. The treated group showed an increase in the G2/M phase (26.50%) compared to control (19.30%), indicating G2/M arrest. Data are representative of three independent experiments ( n = 3).

Article Snippet: The T47D human breast cancer cell line was obtained from the Pasteur Institute of Iran.

Techniques: Control

Journal: Scientific Reports

Article Title: Development of a pH-responsive pegylated chitosan nanocarrier for targeted delivery of 17-AAG and synergistic therapy in HER2 + breast cancer

doi: 10.1038/s41598-025-30507-2

Figure Lengend Snippet: qRT-PCR analysis of HSP90 and β-actin gene expression in T47D cells after 72 h treatment with 17-AAG-loaded PEG-CS NPs. A Melting curves for HSP90 (Tm = 78.2 °C) and β-actin (Tm = 83.9 °C), showing single sharp peaks that confirm the specificity of amplification and absence of primer-dimers. Data are representative of three independent experiments ( n = 3). B Amplification curves for HSP90 (purple line) and β-actin (blue line) genes, showing the cycle threshold (Ct) values used for relative quantification of gene expression.

Article Snippet: The T47D human breast cancer cell line was obtained from the Pasteur Institute of Iran.

Techniques: Quantitative RT-PCR, Gene Expression, Amplification, Quantitative Proteomics

Journal: Cell Reports Medicine

Article Title: Co-targeting CDK4/6 enhances anti-cancer activity and alleviates immune-related adverse events of anti-PD-1 antibody for breast cancer

doi: 10.1016/j.xcrm.2025.102429

Figure Lengend Snippet: DEHP promotes immune evasion in breast cancer cells by inducing PD-L1 expression via ERβ-dependent transcriptional activation (A and B) The changes in mRNA expression in response to DEHP treatment were examined in RNA sequencing analysis, and the most significant pathways in HALLMARK and Gene Ontology (GO) related to regulation of immunity were analyzed. (C and D) Induction of PD-L1 expression by DEHP treatment for 24 h in breast MCF-10A epithelial cells was observed in western blot analysis with quantitation and normalization with the level of β-actin (C) or immunofluorescence (D). Scale bars, 25 μm. (E) The induction of PD-L1-positive population of MCF-10A cells by DEHP was determined by flow cytometry. (F) Transcriptional activation of PD-L1 promoter-reporter gene in response to DEHP treatment. PD-L1 -Luc was co-transfected with β-galactosidase into MCF-7 cells. The luminescence signal from the PD-L1 -Luc reporter was normalized with β-galactosidase activity ( n = 3). (G) Predicted transcription factors binding to PD-L1 promoter were analyzed by using the Jaspar database. (H) The correlation between transcription factors with PD-L1 expression in TCGA database was analyzed by using TIMER2.0. (I and J) Detection of PD-L1, ERα, and ERβ expression in breast MCF-7, T47D, MDA-MB-231, and 4T1 cancer cells treated with DEHP for 24 h was performed in western blot analysis. (K) The downregulation of PD-L1 by ERβ silence was examined in western blot. (L and M) MDA-MB-231 cells were infected with the viral shERβ and the PD-L1 mRNA (L), and promoter (M) levels were measured in quantitative reverse-transcription PCR and luciferase assays, respectively. (N) Representative sequences of the PD-L1 promoter with different mutations in the transcription factor binding sites and primers for ChIP assay. (O) Mutation of ERβ-binding sites decreased the DEHP-induced PD-L1 promoter activity in MDA-MB-231 cancer cells, and luciferase activity was normalized with β-gal activity. (P) DEHP (10 μM) induced chromatin-binding affinity of ERβ preferentially on ESR2#2 and ESR2#3 of the PD-L1 promoter in MDA-MB-231 cancer cells in ChIP assays. Data are shown as mean ± SEM. Data in (E), (F), (L), (M), (O), and (P) were representative of three experiments and were shown as the mean ± SD. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001 versus the control group, Student’s unpaired t test.

Article Snippet: T47D human breast cancer cells , ATCC , RRID: CVCL_0553.

Techniques: Expressing, Activation Assay, RNA Sequencing, Western Blot, Quantitation Assay, Immunofluorescence, Flow Cytometry, Transfection, Activity Assay, Binding Assay, Infection, Reverse Transcription, Luciferase, Mutagenesis, Control