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ATCC mda mb 231

FAME-CRISPR improves CRISPR/Cas9 gene editing efficiency through HDACi mediated chromatin relaxation and precise eVLP delivery (A) shows a brief schematic of the major steps required to improve editing efficacy using FAME-CRISPR workflow. (B), (C), (D), and (E) show representative results <t>obtained</t> <t>from</t> <t>MDA-MB-231</t> one of the utilized cell lines from the original FAME-CRISPR study ([60nM panobinostat] and [1.5 μM belinostat]) (n = 3 biological replicates for all conditions, and error bars reflect standard deviation). Results and raw data for MDA-MB-231 and other tested cell lines are available in the original study and data availability statement section of STAR Protocols.

Mda Mb 231, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 24214 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Protocol for enhancing CRISPR-Cas9 genome editing using histone deacetylase inhibition and engineered virus-like particle delivery"

Article Title: Protocol for enhancing CRISPR-Cas9 genome editing using histone deacetylase inhibition and engineered virus-like particle delivery

Journal: STAR Protocols

doi: 10.1016/j.xpro.2026.104493

Figure Legend Snippet: FAME-CRISPR improves CRISPR/Cas9 gene editing efficiency through HDACi mediated chromatin relaxation and precise eVLP delivery (A) shows a brief schematic of the major steps required to improve editing efficacy using FAME-CRISPR workflow. (B), (C), (D), and (E) show representative results obtained from MDA-MB-231 one of the utilized cell lines from the original FAME-CRISPR study ([60nM panobinostat] and [1.5 μM belinostat]) (n = 3 biological replicates for all conditions, and error bars reflect standard deviation). Results and raw data for MDA-MB-231 and other tested cell lines are available in the original study and data availability statement section of STAR Protocols.

Techniques Used: CRISPR, Standard Deviation

Image Search Results

Journal: STAR Protocols

Article Title: Protocol for enhancing CRISPR-Cas9 genome editing using histone deacetylase inhibition and engineered virus-like particle delivery

doi: 10.1016/j.xpro.2026.104493

Figure Lengend Snippet: FAME-CRISPR improves CRISPR/Cas9 gene editing efficiency through HDACi mediated chromatin relaxation and precise eVLP delivery (A) shows a brief schematic of the major steps required to improve editing efficacy using FAME-CRISPR workflow. (B), (C), (D), and (E) show representative results obtained from MDA-MB-231 one of the utilized cell lines from the original FAME-CRISPR study ([60nM panobinostat] and [1.5 μM belinostat]) (n = 3 biological replicates for all conditions, and error bars reflect standard deviation). Results and raw data for MDA-MB-231 and other tested cell lines are available in the original study and data availability statement section of STAR Protocols.

Article Snippet: MDA-MB-231 , ATCC , #HTB-26.

Techniques: CRISPR, Standard Deviation

CEP exerts cytotoxicity in TNBC cells. (A) Chemical structure of CEP. (B) CEP inhibited TNBC cell viability. The effect of CEP treatment on TNBC cell viability after 24, 48 and 72 h. (C) CEP inhibited clonogenicity of MDA-MB-231 and Hs578T cells. n=3; *P < 0.05, **P < 0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; TNBC, triple-negative breast cancer.

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP exerts cytotoxicity in TNBC cells. (A) Chemical structure of CEP. (B) CEP inhibited TNBC cell viability. The effect of CEP treatment on TNBC cell viability after 24, 48 and 72 h. (C) CEP inhibited clonogenicity of MDA-MB-231 and Hs578T cells. n=3; *P < 0.05, **P < 0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; TNBC, triple-negative breast cancer.

Article Snippet: The TNBC cell lines MDA-MB-231 (cat. no. CL-0150; Procell Life Science & Technology Co., Ltd.) and Hs578T (cat. no. CL-0114; Procell Life Science & Technology Co., Ltd.) were cultured in high-glucose DMEM medium (cat. no. C11965500BT; Gibco; Thermo Fisher Scientific, Inc.), supplemented with 10% fetal bovine serum (cat. no. 164210; Procell Life Science & Technology Co., Ltd.) and 1% penicillin/streptomycin (cat. no. 15140122; Gibco; Thermo Fisher Scientific, Inc.).

Techniques: Control

CEP induces apoptosis in triple-negative breast cancer cells. Flow cytometric quantification of apoptosis induced by CEP in (A) MDA-MB-231 and (B) Hs578T cells (n=3; 48 h). **P<0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; ns, not significant.

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP induces apoptosis in triple-negative breast cancer cells. Flow cytometric quantification of apoptosis induced by CEP in (A) MDA-MB-231 and (B) Hs578T cells (n=3; 48 h). **P<0.01 and ***P < 0.001 vs. control. CEP, cepharanthine; ns, not significant.

Techniques: Control

CEP induces ΔΨm loss in triple-negative breast cancer cells. (A) MDA-MB-231 (10 µM; n=3; 24 h) and (B) Hs578T cells (4 µM; n=3; 24 h). Scale bar, 100 µM. CEP, cepharanthine.

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP induces ΔΨm loss in triple-negative breast cancer cells. (A) MDA-MB-231 (10 µM; n=3; 24 h) and (B) Hs578T cells (4 µM; n=3; 24 h). Scale bar, 100 µM. CEP, cepharanthine.

Techniques:

CEP upregulates NOXA and downregulates Bcl-2 expression in triple-negative breast cancer cells. CEP upregulated NOXA and downregulated Bcl-2 expression in (A) MDA-MB-231 cells (n=3; 24 h) and (B) Hs578T cells (n=3; 24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; NOXA, phorbol-12-myristate-13-acetate-induced protein 1; ns, not significant.

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP upregulates NOXA and downregulates Bcl-2 expression in triple-negative breast cancer cells. CEP upregulated NOXA and downregulated Bcl-2 expression in (A) MDA-MB-231 cells (n=3; 24 h) and (B) Hs578T cells (n=3; 24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; NOXA, phorbol-12-myristate-13-acetate-induced protein 1; ns, not significant.

Techniques: Expressing, Control

Proteomic profiling of MDA-MB-231 cells following CEP treatment. (A) The 20 most significantly downregulated Gene Ontology cellular components with CEP treatment. (B) Significantly downregulated Kyoto Encyclopedia of Genes and Genomes pathways with CEP treatment. CEP, cepharanthine.

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: Proteomic profiling of MDA-MB-231 cells following CEP treatment. (A) The 20 most significantly downregulated Gene Ontology cellular components with CEP treatment. (B) Significantly downregulated Kyoto Encyclopedia of Genes and Genomes pathways with CEP treatment. CEP, cepharanthine.

Techniques:

CEP treatment activates TFEB in triple-negative breast cancer cells. (A) CEP triggers TFEB nuclear translocation in MDA-MB-231 cells (10 µM; 24 h). (B) CEP triggers TFEB nuclear translocation in Hs578T cells (4 µM; 24 h). Scale bar, 25 µm; n=5. **P<0.01 vs. control. TFEB, transcription factor EB; CEP, cepharanthine.

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP treatment activates TFEB in triple-negative breast cancer cells. (A) CEP triggers TFEB nuclear translocation in MDA-MB-231 cells (10 µM; 24 h). (B) CEP triggers TFEB nuclear translocation in Hs578T cells (4 µM; 24 h). Scale bar, 25 µm; n=5. **P<0.01 vs. control. TFEB, transcription factor EB; CEP, cepharanthine.

Techniques: Translocation Assay, Control

CEP does not induce LMP, increase lysosomal pH or destabilize lysosomal membrane-bound enzymes in triple-negative breast cancer cells. (A) CEP does not induce LMP, as evidenced by a dispersion of dextran, in MDA-MB-231 (10 µM; 24 h) and Hs578T cells (4 µM; 24 h). Scale bar, 25 µm. (B) CEP does not elevate lysosomal pH in the MDA-MB-231 (10 µM; 24 h) and Hs578T cell lines (4 µM; 24 h). Scale bar, 25 µm. (C) CEP does not induce lysosomal membrane-bound enzymes degradation in the MDA-MB-231 (10 µM; n=3; 24 h) and Hs578T cell lines (4 µM; n=3; 24 h). CEP, cepharanthine; ASAH1, acid ceramidase; SMPD1, sphingomyelin phosphodiesterase; ns, not significant.

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP does not induce LMP, increase lysosomal pH or destabilize lysosomal membrane-bound enzymes in triple-negative breast cancer cells. (A) CEP does not induce LMP, as evidenced by a dispersion of dextran, in MDA-MB-231 (10 µM; 24 h) and Hs578T cells (4 µM; 24 h). Scale bar, 25 µm. (B) CEP does not elevate lysosomal pH in the MDA-MB-231 (10 µM; 24 h) and Hs578T cell lines (4 µM; 24 h). Scale bar, 25 µm. (C) CEP does not induce lysosomal membrane-bound enzymes degradation in the MDA-MB-231 (10 µM; n=3; 24 h) and Hs578T cell lines (4 µM; n=3; 24 h). CEP, cepharanthine; ASAH1, acid ceramidase; SMPD1, sphingomyelin phosphodiesterase; ns, not significant.

Techniques: Membrane, Dispersion

CEP binds to and inhibits lysosomal enzymes. (A) Structurally altered peptides in the MDA-MB-231 cell line upon CEP treatment (10 µM, 1 h; FC >1.5 or <0.667, false discovery rate <1, P<0.01; n=3). (B) CEP treatment suppresses the maturation of CTSB and CTSD (24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; FC, fold change; CTSD, cathepsin D; CTSB, cathepsin B; pro-CTSB pro-cathepsin B; pro-CTSD, pro-cathepsin D; i-CTSB, inactive cathepsin B; m-CTSB, mature cathepsin B; m-CTSD, mature cathepsin D.

Journal: Molecular Medicine Reports

Article Title: Cepharanthine inhibits lysosomes and induces apoptosis in triple-negative breast cancer cells

doi: 10.3892/mmr.2026.13899

Figure Lengend Snippet: CEP binds to and inhibits lysosomal enzymes. (A) Structurally altered peptides in the MDA-MB-231 cell line upon CEP treatment (10 µM, 1 h; FC >1.5 or <0.667, false discovery rate <1, P<0.01; n=3). (B) CEP treatment suppresses the maturation of CTSB and CTSD (24 h). *P<0.05, **P<0.01 and ***P<0.001 vs. control. CEP, cepharanthine; FC, fold change; CTSD, cathepsin D; CTSB, cathepsin B; pro-CTSB pro-cathepsin B; pro-CTSD, pro-cathepsin D; i-CTSB, inactive cathepsin B; m-CTSB, mature cathepsin B; m-CTSD, mature cathepsin D.

Techniques: Control

Macrophage-targeted GO-EDM-DTX-Vad induces M2-to-M1 repolarization and limits TNBC cell proliferation and migration. (A) After incubation of M2-polarized macrophages with the nanocomposites for 24 h, CD206 and CD86 were quantified by flow cytometry. (B) After co-treatment of M0 RAW264.7 cells with IL-4/IL-13 and the nanocomposites for 48 h, CD206 and CD86 were quantified by flow cytometry. (C) RT-qPCR of CD86, iNOS, CD206 and IL-10 expression. (D) RAW264.7 immunoblots of STING axis including TBK1, phospho-TBK1, IRF3 and phospho-IRF3, with GAPDH as a reference. (E) CLSM images of RAW264.7 uptake of RhoB–GO-EDM-DTX-Vad (nuclei, blue; nanocomposites, red; scale bar, 100 μm). (F) ELISA of TGF-β, IL-10 and TNF-α in culture supernatants. (G) Schematic of the in vitro workflow for generating macrophage-conditioned media and assessing CM-driven tumor cell functions. (H, I) Colony formation (H) and EdU flow-cytometry analyses (I) of 4T1 and MDA-MB-231 cells after treatment with the indicated macrophage-CM. Groups: G1, PBS; G2, GO-EDM; G3, GO-EDM-DTX; G4, GO-EDM-Vad; G5, GO-EDM-DTX-Vad; G6, GO-EDM-DTX-Vad + NIR. Data are mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; ns, not significant.

Journal: Materials Today Bio

Article Title: Mannosylated graphene oxide nanotherapeutics co-delivering docetaxel and a STING agonist reprogram myeloid cells and potentiate antitumor immunity

doi: 10.1016/j.mtbio.2026.103086

Figure Lengend Snippet: Macrophage-targeted GO-EDM-DTX-Vad induces M2-to-M1 repolarization and limits TNBC cell proliferation and migration. (A) After incubation of M2-polarized macrophages with the nanocomposites for 24 h, CD206 and CD86 were quantified by flow cytometry. (B) After co-treatment of M0 RAW264.7 cells with IL-4/IL-13 and the nanocomposites for 48 h, CD206 and CD86 were quantified by flow cytometry. (C) RT-qPCR of CD86, iNOS, CD206 and IL-10 expression. (D) RAW264.7 immunoblots of STING axis including TBK1, phospho-TBK1, IRF3 and phospho-IRF3, with GAPDH as a reference. (E) CLSM images of RAW264.7 uptake of RhoB–GO-EDM-DTX-Vad (nuclei, blue; nanocomposites, red; scale bar, 100 μm). (F) ELISA of TGF-β, IL-10 and TNF-α in culture supernatants. (G) Schematic of the in vitro workflow for generating macrophage-conditioned media and assessing CM-driven tumor cell functions. (H, I) Colony formation (H) and EdU flow-cytometry analyses (I) of 4T1 and MDA-MB-231 cells after treatment with the indicated macrophage-CM. Groups: G1, PBS; G2, GO-EDM; G3, GO-EDM-DTX; G4, GO-EDM-Vad; G5, GO-EDM-DTX-Vad; G6, GO-EDM-DTX-Vad + NIR. Data are mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; ns, not significant.

Article Snippet: 4T1 and MDA-MB-231 cells were treated with the indicated nanocomposites for 24 h. The apoptosis was quantified by Annexin V-FITC/PI staining (Elabscience, Wuhan, China) followed by flow cytometry, and cell viability was visualized by Calcein-AM/PI live/dead staining (Servicebio, Wuhan, China) using CLSM.

Techniques: Migration, Incubation, Flow Cytometry, Quantitative RT-PCR, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, In Vitro

GO-EDM-DTX-Vad combined with NIR induces TNBC cell death, apoptosis and immunogenic cell death. (A, B) Calcein-AM/PI live/dead staining of 4T1 (A) and MDA-MB-231 (B) cells (live, green; dead, red; scale bar, 200 μm). (C, D) Annexin V/PI apoptosis plots for 4T1 (C) and MDA-MB-231 (D) cells. (E, F) Quantification of viable and early/late apoptotic 4T1 cells. (H, I) Quantification of viable and early/late apoptotic MDA-MB-231 cells. (G, J) Dose–response viability curves after 48 h treatment with free DTX or GO-EDM-DTX-Vad in 4T1 (G) and MDA-MB-231 (J). (K, L) Immunofluorescence of CRT exposure and HMGB1 release after 24 h treatment in 4T1 (K) and MDA-MB-231 (L) cells (nuclei, blue; CRT/HMGB1, green; scale bar, 100 μm). (M) Schematic of the ICD-to-DC maturation assay. (N–P) Frequencies of CD40 + , CD80 + and CD86 + DCs after co-culture. Data are mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; ns, not significant.

Journal: Materials Today Bio

Article Title: Mannosylated graphene oxide nanotherapeutics co-delivering docetaxel and a STING agonist reprogram myeloid cells and potentiate antitumor immunity

doi: 10.1016/j.mtbio.2026.103086

Figure Lengend Snippet: GO-EDM-DTX-Vad combined with NIR induces TNBC cell death, apoptosis and immunogenic cell death. (A, B) Calcein-AM/PI live/dead staining of 4T1 (A) and MDA-MB-231 (B) cells (live, green; dead, red; scale bar, 200 μm). (C, D) Annexin V/PI apoptosis plots for 4T1 (C) and MDA-MB-231 (D) cells. (E, F) Quantification of viable and early/late apoptotic 4T1 cells. (H, I) Quantification of viable and early/late apoptotic MDA-MB-231 cells. (G, J) Dose–response viability curves after 48 h treatment with free DTX or GO-EDM-DTX-Vad in 4T1 (G) and MDA-MB-231 (J). (K, L) Immunofluorescence of CRT exposure and HMGB1 release after 24 h treatment in 4T1 (K) and MDA-MB-231 (L) cells (nuclei, blue; CRT/HMGB1, green; scale bar, 100 μm). (M) Schematic of the ICD-to-DC maturation assay. (N–P) Frequencies of CD40 + , CD80 + and CD86 + DCs after co-culture. Data are mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; ns, not significant.

Techniques: Staining, Immunofluorescence, Co-Culture Assay

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 (*).

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

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 (*).

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

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.

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

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.

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

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.

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

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.

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

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