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human breast cancer cell line hs578t (ATCC)

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ATCC human breast cancer cell line hs578t
Human Breast Cancer Cell Line Hs578t, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 2317 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+breast+cancer+cell+line+hs578t/Hs+578T/pm42020392-214-1-10
Average 97 stars, based on 2317 article reviews

human breast cancer cell line hs578t - by Bioz Stars, 2026-09

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Article Title: Cancer stem cell populations are resistant to 5-aminolevulinic acid- photodynamic therapy (5-ALA-PDT)
Article Snippet: .. Methods Page 4/16 Cell culture The human lung cancer cell line H1299, human breast cancer cell line Hs578T and human colon cancer cell lines DLD-1, were purchased from the American Type Culture Collection (ATCC). .. All cells were cultured in high-glucose Dulbecco’s modi ed Eagle’s medium (DMEM) (Corning, MA) supplemented with 10% fetal bovine serum (HyClone, Cytiva), 1 mM sodium pyruvate (Life Technologies) and antibioticantimycotic (Thermo Scienti c).

Article Title: Cytochalasins Suppress 3D Migration of ECM-Embedded Tumoroids at Non-Toxic Concentrations
Article Snippet: .. The human breast cancer cell line Hs578T (ATCC, #HTB-126, Manassas, VA, USA), the human melanoma cell line MV3 [ ], and hTERT-immortalized human fibroblasts (ATCC, #CRL-4001) were cultured in high-glucose Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco, 11504496, Waltham, MA, USA) containing L-Glutamine and Sodium Pyruvate, supplemented with 10% fetal calf serum (Thermo Scientific, Waltham, MA, USA) and 25 μg/mL penicillin/streptomycin in a humidified incubator at 37 °C with 5% CO 2 . .. Dox-inducible Hs578T-Cas9 and MV3-Cas9 cell lines were generated using an Edit-R Inducible Lentiviral hEF1α-Blast-Cas9 Nuclease Plasmid DNA (Dharmacon, CAS11229 , Lafayette, CO, USA).

Article Title: Trifluoperazine causes mast cell apoptosis through a secretory granule-mediated pathway
Article Snippet: Primary human small airway epithelial cells (HSAECs) (PCS-301-010) were obtained from ATCC and cultured in Airway Epithelial Cell Basal Medium (ATCC) containing a Bronchial Epithelial Cell Growth Kit (ATCC) and penicillin-streptomycin (100 U/mL, 100 μg/mL). .. Triple-negative human breast cancer cell line Hs578T was obtained from ATCC (HTB-126) and cultured at 37 °C in 5% CO 2 in DMEM (Invitrogen) supplemented with 10% FBS, penicillin-streptomycin (50 μg/ml, 60 μg/ml), and 2 mM L-glutamine (Sigma-Aldrich). ..

Article Title: Trifluoperazine causes mast cell apoptosis through a secretory granule-mediated pathway.
Article Snippet: Primary human small airway epithelial cells (HSAECs) (PCS-301-010) were obtained from ATCC and cultured in Airway Epithelial Cell Basal Medium (ATCC) containing a Bronchial Epithelial Cell Growth Kit (ATCC) and penicillin-streptomycin (100 U/mL, 100 μg/mL). .. Triple-negative human breast cancer cell line Hs578T was obtained from ATCC (HTB-126) and cultured at 37 °C in 5% CO2 in DMEM (Invitrogen) supplemented with 10% FBS, penicillinstreptomycin (50 μg/ml, 60 μg/ml), and 2 mM L-glutamine (Sigma-Aldrich). ..

Article Title: Cytochalasins Suppress 3D Migration of ECM-Embedded Tumoroids at Non-Toxic Concentrations.
Article Snippet: .. The human breast cancer cell line Hs578T (ATCC, #HTB-126, Manassas, VA, USA), the human melanoma cell line MV3 [50], and hTERT-immortalized human fibroblasts (ATCC, #CRL-4001) were cultured in high-glucose Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco, 11504496, Waltham, MA, USA) containing L-Glutamine and Sodium Pyruvate, supplemented with 10% fetal calf serum (Thermo Scientific, Waltham, MA, USA) and 25 μg/mL penicillin/streptomycin in a humidified incubator at 37 ◦C with 5% CO2. .. Dox-inducible Hs578T-Cas9 and MV3-Cas9 cell lines were generated using an Edit-R Inducible Lentiviral hEF1α-Blast-Cas9 Nuclease Plasmid DNA (Dharmacon, CAS11229, Lafayette, CO, USA).

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Hypoxia promotes enrichment and DNA damage-independent oxidative activation of ataxia telangiectasia mutated. A: Flow cytometry analysis of CD44+/CD24- cell populations in Hs578T and MDA-MB-231 cells after exposure to hypoxia or normoxia; B: Quantitative reverse transcriptase polymerase chain reaction analysis of cancer stem cells-associated genes ( c-Myc , octamer-binding protein 4, Kruppel-like factor 4, sex-determining region Y-box 2, NANOG ) in mammosphere cultures under hypoxia; C-E: Western blot analysis of phosphorylated ataxia telangiectasia mutated, γH2AX, and 53BP1 in Hs578T and MDA-MB-231 cancer stem cells under normoxia, hypoxia, or H 2 O 2 treatment. Data were presented as mean ± SD ( n = 3). a P < 0.05; b P < 0.01; ns: not significant. KLF4: Kruppel-like factor 4; SOX2: Sex-determining region Y-box 2; OCT4: Octamer-binding protein 4; p-ATM: Phosphorylated ataxia telangiectasia mutated.

Journal: World Journal of Stem Cells

Article Title: Hypoxia facilitates triple-negative breast cancer stem cells enrichment and stemness maintenance through oxidized ataxia telangiectasia mutated-induced one-carbon metabolism

doi: 10.4252/wjsc.v18.i1.112278

Figure Lengend Snippet: Hypoxia promotes enrichment and DNA damage-independent oxidative activation of ataxia telangiectasia mutated. A: Flow cytometry analysis of CD44+/CD24- cell populations in Hs578T and MDA-MB-231 cells after exposure to hypoxia or normoxia; B: Quantitative reverse transcriptase polymerase chain reaction analysis of cancer stem cells-associated genes ( c-Myc , octamer-binding protein 4, Kruppel-like factor 4, sex-determining region Y-box 2, NANOG ) in mammosphere cultures under hypoxia; C-E: Western blot analysis of phosphorylated ataxia telangiectasia mutated, γH2AX, and 53BP1 in Hs578T and MDA-MB-231 cancer stem cells under normoxia, hypoxia, or H 2 O 2 treatment. Data were presented as mean ± SD ( n = 3). a P < 0.05; b P < 0.01; ns: not significant. KLF4: Kruppel-like factor 4; SOX2: Sex-determining region Y-box 2; OCT4: Octamer-binding protein 4; p-ATM: Phosphorylated ataxia telangiectasia mutated.

Article Snippet: The human breast cancer cell lines Hs578T and MDA-MB-231 were acquired from the American Type Culture Collection.

Techniques: Activation Assay, Flow Cytometry, Reverse Transcription, Polymerase Chain Reaction, Binding Assay, Western Blot

Oxidized ataxia telangiectasia mutated promotes serine hydroxymethyltransferase 2 and methylenetetrahydrofolate dehydrogenase 2 expression through c-Myc. A and B: Western blot analysis of phosphorylated ataxia telangiectasia mutated, c-Myc, serine hydroxymethyltransferase 2 (SHMT2), and methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) in Hs578T and MDA-MB-231 cells after treatment with Ku60019 and ataxia telangiectasia mutated knockdown; C: Consensus c-Myc binding motif; D: Schematic representation of predicted c-Myc binding sites in the human MTHFD2 and SHMT2 promoter regions; E: Luciferase assay showed SHMT2 and MTHFD2 relative luciferase activity; F: Representative chromatin immunoprecipitation (ChIP)-polymerase chain reaction (PCR) showing c-Myc occupancy at the MTHFD2 and SHMT2 promoters; input and immunoglobulin G served as controls; G and H: ChIP-quantitative PCR analysis demonstrating c-Myc enrichment at the MTHFD2 (G) and SHMT2 (H) promoters in Hs578T and MDA-MB-231 cells. ChIP-quantitative PCR enrichment expressed as % input relative to immunoglobulin G. Data were presented as mean ± SD ( n = 3). a P < 0.05; b P < 0.01. p-ATM: Phosphorylated ataxia telangiectasia mutated; MTHFD2: Methylenetetrahydrofolate dehydrogenase 2; SHMT2: Serine hydroxymethyltransferase 2; IgG: Immunoglobulin G.

Journal: World Journal of Stem Cells

Article Title: Hypoxia facilitates triple-negative breast cancer stem cells enrichment and stemness maintenance through oxidized ataxia telangiectasia mutated-induced one-carbon metabolism

doi: 10.4252/wjsc.v18.i1.112278

Figure Lengend Snippet: Oxidized ataxia telangiectasia mutated promotes serine hydroxymethyltransferase 2 and methylenetetrahydrofolate dehydrogenase 2 expression through c-Myc. A and B: Western blot analysis of phosphorylated ataxia telangiectasia mutated, c-Myc, serine hydroxymethyltransferase 2 (SHMT2), and methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) in Hs578T and MDA-MB-231 cells after treatment with Ku60019 and ataxia telangiectasia mutated knockdown; C: Consensus c-Myc binding motif; D: Schematic representation of predicted c-Myc binding sites in the human MTHFD2 and SHMT2 promoter regions; E: Luciferase assay showed SHMT2 and MTHFD2 relative luciferase activity; F: Representative chromatin immunoprecipitation (ChIP)-polymerase chain reaction (PCR) showing c-Myc occupancy at the MTHFD2 and SHMT2 promoters; input and immunoglobulin G served as controls; G and H: ChIP-quantitative PCR analysis demonstrating c-Myc enrichment at the MTHFD2 (G) and SHMT2 (H) promoters in Hs578T and MDA-MB-231 cells. ChIP-quantitative PCR enrichment expressed as % input relative to immunoglobulin G. Data were presented as mean ± SD ( n = 3). a P < 0.05; b P < 0.01. p-ATM: Phosphorylated ataxia telangiectasia mutated; MTHFD2: Methylenetetrahydrofolate dehydrogenase 2; SHMT2: Serine hydroxymethyltransferase 2; IgG: Immunoglobulin G.

Article Snippet: The human breast cancer cell lines Hs578T and MDA-MB-231 were acquired from the American Type Culture Collection.

Techniques: Expressing, Western Blot, Knockdown, Binding Assay, Luciferase, Activity Assay, Chromatin Immunoprecipitation, Polymerase Chain Reaction, Real-time Polymerase Chain Reaction

Serine hydroxymethyltransferase 2 and methylenetetrahydrofolate dehydrogenase 2 promote cancer stem cells enrichment and stemness maintenance in triple-negative breast cancer. A: Effects of serine hydroxymethyltransferase 2 knockdown on mammosphere formation, size, and number in Hs578T and MDA-MB-231 cancer stem cells; B: Effects of methylenetetrahydrofolate dehydrogenase 2 knockdown on mammosphere formation, size, and number; C and D: Western blot analysis of stemness-associated proteins Kruppel-like factor 4 and sex-determining region Y-box 2 after serine hydroxymethyltransferase 2 or methylenetetrahydrofolate dehydrogenase 2 knockdown. Scale bar: 200 μm. Data were presented as mean ± SD ( n = 3). a P < 0.05. MTHFD2: Methylenetetrahydrofolate dehydrogenase 2; SHMT2: Serine hydroxymethyltransferase 2; KLF4: Kruppel-like factor 4; SOX2: Sex-determining region Y-box 2.

Journal: World Journal of Stem Cells

Article Title: Hypoxia facilitates triple-negative breast cancer stem cells enrichment and stemness maintenance through oxidized ataxia telangiectasia mutated-induced one-carbon metabolism

doi: 10.4252/wjsc.v18.i1.112278

Figure Lengend Snippet: Serine hydroxymethyltransferase 2 and methylenetetrahydrofolate dehydrogenase 2 promote cancer stem cells enrichment and stemness maintenance in triple-negative breast cancer. A: Effects of serine hydroxymethyltransferase 2 knockdown on mammosphere formation, size, and number in Hs578T and MDA-MB-231 cancer stem cells; B: Effects of methylenetetrahydrofolate dehydrogenase 2 knockdown on mammosphere formation, size, and number; C and D: Western blot analysis of stemness-associated proteins Kruppel-like factor 4 and sex-determining region Y-box 2 after serine hydroxymethyltransferase 2 or methylenetetrahydrofolate dehydrogenase 2 knockdown. Scale bar: 200 μm. Data were presented as mean ± SD ( n = 3). a P < 0.05. MTHFD2: Methylenetetrahydrofolate dehydrogenase 2; SHMT2: Serine hydroxymethyltransferase 2; KLF4: Kruppel-like factor 4; SOX2: Sex-determining region Y-box 2.

Article Snippet: The human breast cancer cell lines Hs578T and MDA-MB-231 were acquired from the American Type Culture Collection.

Techniques: Knockdown, Western Blot

Fig. 2. NID1 downregulated cell migration and EMT marker expression. (A) Wound-healing assay of the MDA-MB-231 and Hs578T NID1-overexpressing cell lines. The healed rate of each wound area was measured at 24 h intervals. (B–C) (B) Transwell migration and (C) invasion assays were performed with the MDA- MB-231 and Hs578T NID1-overexpressing cell lines. (D) Immunofluorescence analysis showed decreased expression of the mesenchymal marker vimentin (scale bar = 100 μm). (E) Western blot analysis of total cell lysate with the indicated antibodies showed decreased expression of EMT marker proteins. (F) RT-qPCR analysis showing the mRNA expression of EMT markers in the indicated cell lines. The values were normalized to the GAPDH level. The data in (A, B, C, and F) are presented as mean ± SD. P values in (A, B, C, and F) were calculated using Student’s t test (* P < 0.05; ** P < 0.005; *** P < 0.0005).

Journal: Scientific reports

Article Title: Nidogen-1 suppresses cell proliferation, migration, and glycolysis via integrin β1-mediated HIF-1α downregulation in triple-negative breast cancer.

doi: 10.1038/s41598-024-84880-5

Figure Lengend Snippet: Fig. 2. NID1 downregulated cell migration and EMT marker expression. (A) Wound-healing assay of the MDA-MB-231 and Hs578T NID1-overexpressing cell lines. The healed rate of each wound area was measured at 24 h intervals. (B–C) (B) Transwell migration and (C) invasion assays were performed with the MDA- MB-231 and Hs578T NID1-overexpressing cell lines. (D) Immunofluorescence analysis showed decreased expression of the mesenchymal marker vimentin (scale bar = 100 μm). (E) Western blot analysis of total cell lysate with the indicated antibodies showed decreased expression of EMT marker proteins. (F) RT-qPCR analysis showing the mRNA expression of EMT markers in the indicated cell lines. The values were normalized to the GAPDH level. The data in (A, B, C, and F) are presented as mean ± SD. P values in (A, B, C, and F) were calculated using Student’s t test (* P < 0.05; ** P < 0.005; *** P < 0.0005).

Article Snippet: The MDA-MB-231 and Hs578T human breast cancer cell lines were obtained from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Migration, Marker, Expressing, Wound Healing Assay, Immunofluorescence, Western Blot, Quantitative RT-PCR

Fig. 5. NID1 suppressed the FAK/Src/NF-κB p65 signaling axis via integrin β1 downregulation. (A) Western blot analysis of total cell lysates with the indicated antibodies. β-actin was used as the loading control. (B) RT- qPCR analysis showing the mRNA expression of ITGB1 in the indicated cell lines. Values were normalized to GAPDH. (C–D) Cycloheximide (CHX) chase assays were performed to measure the degradation of integrin β1 in the (C) MDA-MB-231 and (D) Hs578T NID1-overexpressing cell lines. Cells were treated with CHX (40 μg/ ml) and harvested at the indicated times. (E) To detect ubiquitinated integrin β1, an immunoprecipitation analysis was performed with anti-integrin β1 antibody after a 24-h incubation with MG132 (10 μM). (F) Western blot analysis of total cell lysates with the indicated antibodies; GAPDH was used as the loading control. (G) Dual luciferase assays were performed using NF-κB-luc constructs. pRL-CMV was used as the internal control. (H) Kaplan–Meier survival analysis of breast cancer patients based on NID1 expression levels. (I) A schematic description of the NID1-mediated signaling pathway in breast cancer cells. Data in (B, C, D, and G) are presented as mean ± SD. P values in (B, C, D, and G) were calculated using Student’s t test; in H, they were calculated with the log-rank test (*P < 0.05; **P < 0.005; ***P < 0.0005).

Journal: Scientific reports

Article Title: Nidogen-1 suppresses cell proliferation, migration, and glycolysis via integrin β1-mediated HIF-1α downregulation in triple-negative breast cancer.

doi: 10.1038/s41598-024-84880-5

Figure Lengend Snippet: Fig. 5. NID1 suppressed the FAK/Src/NF-κB p65 signaling axis via integrin β1 downregulation. (A) Western blot analysis of total cell lysates with the indicated antibodies. β-actin was used as the loading control. (B) RT- qPCR analysis showing the mRNA expression of ITGB1 in the indicated cell lines. Values were normalized to GAPDH. (C–D) Cycloheximide (CHX) chase assays were performed to measure the degradation of integrin β1 in the (C) MDA-MB-231 and (D) Hs578T NID1-overexpressing cell lines. Cells were treated with CHX (40 μg/ ml) and harvested at the indicated times. (E) To detect ubiquitinated integrin β1, an immunoprecipitation analysis was performed with anti-integrin β1 antibody after a 24-h incubation with MG132 (10 μM). (F) Western blot analysis of total cell lysates with the indicated antibodies; GAPDH was used as the loading control. (G) Dual luciferase assays were performed using NF-κB-luc constructs. pRL-CMV was used as the internal control. (H) Kaplan–Meier survival analysis of breast cancer patients based on NID1 expression levels. (I) A schematic description of the NID1-mediated signaling pathway in breast cancer cells. Data in (B, C, D, and G) are presented as mean ± SD. P values in (B, C, D, and G) were calculated using Student’s t test; in H, they were calculated with the log-rank test (*P < 0.05; **P < 0.005; ***P < 0.0005).

Article Snippet: The MDA-MB-231 and Hs578T human breast cancer cell lines were obtained from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Western Blot, Control, Quantitative RT-PCR, Expressing, Immunoprecipitation, Incubation, Luciferase, Construct

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human breast cancer cell line hs578t (ATCC)

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