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ATCC hs578t
Hs578t, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 2306 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hs578t/10__1016_slash_j__biosx__2026__100805-74-2-10?v=ATCC
Average 97 stars, based on 2306 article reviews

hs578t - by Bioz Stars, 2026-08

97/100 stars

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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

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

Cell viability (MTT assay) of HUVEC (A) and HS578T cells (B) treated for 48 h with commercial DTX or the DTX:γ-CD complex. Results expressed as mean ± SD ( n = 6). Statistical analysis by two-way ANOVA plus Tukey–Kramer post hoc: * p < 0.05; ** p < 0.01; *** p < 0.001, **** p < 0.0001.

Journal: ACS Omega

Article Title: Complexation of the Antineoplastic Docetaxel with γ‑Cyclodextrin Significantly Improves Its Solubility and In Vitro Safety

doi: 10.1021/acsomega.5c10596

Figure Lengend Snippet: Cell viability (MTT assay) of HUVEC (A) and HS578T cells (B) treated for 48 h with commercial DTX or the DTX:γ-CD complex. Results expressed as mean ± SD ( n = 6). Statistical analysis by two-way ANOVA plus Tukey–Kramer post hoc: * p < 0.05; ** p < 0.01; *** p < 0.001, **** p < 0.0001.

Article Snippet: Human umbilical vein endothelial cells (HUVEC, ATCC PCS-100–010) and human breast cancer cells HS578T (ATCC HTB-126) were used in this study.

Techniques: MTT Assay

A. Western blot confirmation of loss of Orai1 expression upon CRISPR/Cas9-mediated KO in MDA-MB-231 and Hs578T cells; shown are pools of three clones maintained individually. B-C. Impairment of SOCE upon Orai1 KO in TNBC cells. SOCE was measured using thapsigargin-induced ER Ca 2+ depletion. Typical profiles are shown on left and quantification of fold-change in peak fluorescence intensity from 3 independent experiments is shown on right. Welch’s t test, ***p<0.001. D-E. Orai1-KO impairs the repair of mechanically induced plasma membrane injury. WT vs. Orai1-KO cells were subjected to mechanical injury to plasma membrane and repair assay was performed as in . Representative confocal images are shown in D and quantified data are shown in E. Scale bar, 200 µm. Data represents mean +/- SEM of three experiments, two-way ANOVA, **,p<0.01. F-G. Orai1-KO impairs the repair of SLO-induced membrane injury. Plasma membrane damage using SLO and the repair assay on MDA-MB-231 ( F ) and Hs578T ( G ) cell lines were as in . Representative confocal images are shown on left. Quantification of PI-stained cells from 3 independent experiments is shown on right. Welch’s t test, ***p<0.001. H-J. Orai1 inhibitors impair plasma membrane repair. Panel H shows Thapsigargin (TG)-induced SOCE measurements (initial peak, Ca 2+ store release in the absence of extracellular Ca 2+ ; second peak, SOCE in the presence of extracellular Ca 2+ ) performed on the indicated cell lines cultured with or without CM4620 (10 μM, 4 hours pretreatment). Note significant SOCE inhibition by CM4620 in WT cells but not in Orai1-KO cells, supporting Orai1-selelctive effect of CM4620. Data represents mean +/- SEM of three experiments, Welch’s t test, ***p<0.001. The I panel shows the impairment of mechanically induced plasma membrane repair by CM4620 in MDA-MB-231. Cells were cultured without or with pretreatment with CM4620 (10 μM) and analyzed for repair as in . Scale bar, 200 µm. Data represents mean +/- SEM of three experiments, two-way ANOVA, **,p<0.01. The J panel shows the impairment of SLO-induced membrane damage in MDA-MB-231. Left panel shows representative FACS analysis of membrane repair in cells without or with CM4620 treatment. Right panel shows quantification of cells that failed to repair (PI staining) from 3 independent experiments. Data represents mean +/-SEM of three experiments. Welch’s t test, ***, p<0.001.

Journal: bioRxiv

Article Title: Orai1 is required for Ca 2+ -dependent plasma membrane repair and mechanoadaptation

doi: 10.64898/2026.05.13.724989

Figure Lengend Snippet: A. Western blot confirmation of loss of Orai1 expression upon CRISPR/Cas9-mediated KO in MDA-MB-231 and Hs578T cells; shown are pools of three clones maintained individually. B-C. Impairment of SOCE upon Orai1 KO in TNBC cells. SOCE was measured using thapsigargin-induced ER Ca 2+ depletion. Typical profiles are shown on left and quantification of fold-change in peak fluorescence intensity from 3 independent experiments is shown on right. Welch’s t test, ***p<0.001. D-E. Orai1-KO impairs the repair of mechanically induced plasma membrane injury. WT vs. Orai1-KO cells were subjected to mechanical injury to plasma membrane and repair assay was performed as in . Representative confocal images are shown in D and quantified data are shown in E. Scale bar, 200 µm. Data represents mean +/- SEM of three experiments, two-way ANOVA, **,p<0.01. F-G. Orai1-KO impairs the repair of SLO-induced membrane injury. Plasma membrane damage using SLO and the repair assay on MDA-MB-231 ( F ) and Hs578T ( G ) cell lines were as in . Representative confocal images are shown on left. Quantification of PI-stained cells from 3 independent experiments is shown on right. Welch’s t test, ***p<0.001. H-J. Orai1 inhibitors impair plasma membrane repair. Panel H shows Thapsigargin (TG)-induced SOCE measurements (initial peak, Ca 2+ store release in the absence of extracellular Ca 2+ ; second peak, SOCE in the presence of extracellular Ca 2+ ) performed on the indicated cell lines cultured with or without CM4620 (10 μM, 4 hours pretreatment). Note significant SOCE inhibition by CM4620 in WT cells but not in Orai1-KO cells, supporting Orai1-selelctive effect of CM4620. Data represents mean +/- SEM of three experiments, Welch’s t test, ***p<0.001. The I panel shows the impairment of mechanically induced plasma membrane repair by CM4620 in MDA-MB-231. Cells were cultured without or with pretreatment with CM4620 (10 μM) and analyzed for repair as in . Scale bar, 200 µm. Data represents mean +/- SEM of three experiments, two-way ANOVA, **,p<0.01. The J panel shows the impairment of SLO-induced membrane damage in MDA-MB-231. Left panel shows representative FACS analysis of membrane repair in cells without or with CM4620 treatment. Right panel shows quantification of cells that failed to repair (PI staining) from 3 independent experiments. Data represents mean +/-SEM of three experiments. Welch’s t test, ***, p<0.001.

Article Snippet: Hs578T cell line (ATCC) was cultured in α-MEM medium supplemented as above plus 1 μg/mL hydrocortisone and 12.5 ng/mL epidermal growth factor (Millipore Sigma, St. Louis, MO).

Techniques: Western Blot, Expressing, CRISPR, Clone Assay, Fluorescence, Clinical Proteomics, Membrane, Staining, Cell Culture, Inhibition

A. TEAD inhibition reduces CAV1 expression. MDA-MB-231 or Hs578T cells cultured without or with the pan-TEAD inhibitor GNE-7883 (10 μM) for 48 hours were analyzed by WB for CAV1 expression; Hsc70, loading control. Fold-change in signals quantified by densitometry and analyzed using Image J are shown on right. Welch’s t test, *, p<0.05; **, p<0.01. B-C. TEAD inhibition reduces the Thapsigargin (TG)-induced SOCE. Cells were pretreated with GNE-7883 (10 μM) for 24 hours. Left, representative plots; right, quantified data from three experiments. Welch’s t test; **p<0.001. D. TEAD inhibition impairs the mechanical force-induced Ca 2+ import. AFM cantilevers were used to apply force and measure Ca 2+ import from the extracellular space using fluorescence intensity of transfected Ca 2+ reporter (R-RECO1.2) as the readout. Cells were pretreated with GNE-7883 (10 μM) for 24 hours where indicated. Data points represent cells analyzed through three independent experiments (n=33). Welch’s t test, ***, p<0.001. E-F. TEAD inhibition impairs the repair of induced plasma membrane injuries. Shown is the impact of GNE-7883 on the repair of mechanically induced ( E ) and SLO-induced ( F ) plasma membrane damage, assessed as in and , respectively. GNE-7883 pre-treatment (10 μM), where indicated, was for 72 hours. Representative confocal images ( E ; top panel) or FACS plots ( F ; right panel) are shown. Quantified data shown are from 3 independent experiments and presented as mean +/- SEM of 3 experiments. Two-way ANOVA or Welch’s t test applied to data in E and F , respectively, *p<0.05. Scale bar, 20 µm.

Journal: bioRxiv

Article Title: Orai1 is required for Ca 2+ -dependent plasma membrane repair and mechanoadaptation

doi: 10.64898/2026.05.13.724989

Figure Lengend Snippet: A. TEAD inhibition reduces CAV1 expression. MDA-MB-231 or Hs578T cells cultured without or with the pan-TEAD inhibitor GNE-7883 (10 μM) for 48 hours were analyzed by WB for CAV1 expression; Hsc70, loading control. Fold-change in signals quantified by densitometry and analyzed using Image J are shown on right. Welch’s t test, *, p<0.05; **, p<0.01. B-C. TEAD inhibition reduces the Thapsigargin (TG)-induced SOCE. Cells were pretreated with GNE-7883 (10 μM) for 24 hours. Left, representative plots; right, quantified data from three experiments. Welch’s t test; **p<0.001. D. TEAD inhibition impairs the mechanical force-induced Ca 2+ import. AFM cantilevers were used to apply force and measure Ca 2+ import from the extracellular space using fluorescence intensity of transfected Ca 2+ reporter (R-RECO1.2) as the readout. Cells were pretreated with GNE-7883 (10 μM) for 24 hours where indicated. Data points represent cells analyzed through three independent experiments (n=33). Welch’s t test, ***, p<0.001. E-F. TEAD inhibition impairs the repair of induced plasma membrane injuries. Shown is the impact of GNE-7883 on the repair of mechanically induced ( E ) and SLO-induced ( F ) plasma membrane damage, assessed as in and , respectively. GNE-7883 pre-treatment (10 μM), where indicated, was for 72 hours. Representative confocal images ( E ; top panel) or FACS plots ( F ; right panel) are shown. Quantified data shown are from 3 independent experiments and presented as mean +/- SEM of 3 experiments. Two-way ANOVA or Welch’s t test applied to data in E and F , respectively, *p<0.05. Scale bar, 20 µm.

Article Snippet: Hs578T cell line (ATCC) was cultured in α-MEM medium supplemented as above plus 1 μg/mL hydrocortisone and 12.5 ng/mL epidermal growth factor (Millipore Sigma, St. Louis, MO).

Techniques: Inhibition, Expressing, Cell Culture, Control, Fluorescence, Transfection, Clinical Proteomics, Membrane

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