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human breast cancer cell line mcf 7 (ATCC)

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ATCC human breast cancer cell line mcf 7
Human Breast Cancer Cell Line Mcf 7, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 34824 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cancerous+cell+lines/MCF7/pmc13101642-243-7-13
Average 99 stars, based on 34824 article reviews

human breast cancer cell line mcf 7 - by Bioz Stars, 2026-09

99/100 stars

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Article Title: Milk supplemented with Okara soymilk.
Article Snippet: Agro-waste industries are focused on the transformation and processing of raw materials derived from agricultural sources, including plant or animal, and contributed to the generation of large amounts of organic residues.. Okara is a major by-product of soymilk and tofu production, a large quantity of okara produced annually pose a significant environmental problem.. Herein, we demonstrated yogurt supplemented with okara at 20 and 30% to enhance milk properties biological benefits as an alternative source.

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Article Title: Forskolin alleviates cisplatin-induced acute renal toxicity in rats.
Article Snippet: Context Renal toxicity correlated with cisplatin administration curbs its clinical application.. Accordingly, the identification of novel protective agents is important.. Forskolin provides anti-inflammatory, anti-oxidant as well as anti-cancer effects.

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Article Title: Designing strategies, structural activity relationship and biological activity of recently developed nitrogen containing heterocyclic compounds as epidermal growth factor receptor tyrosinase inhibitors
Article Snippet: Cancer cells have the ability of dysregulation and autonomous proliferation due to unchecked production of definite molecules.. These molecules are involved in the cell growth (growth factor) or through an irregular and boosted expression of specific proteins (growth factor receptors) on the cell membranes to which growth factors selectively bind.. Both phenomena activate a sequence of intracellular indications that eventually lead to the proliferation of cancer cells, initiation of angiogenesis, and metastasis.

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Article Title: The Use of the QbD Approach to Optimize the Co-Loading of Simvastatin and Doxorubicin in Liposomes for a Synergistic Anticancer Effect.
Article Snippet: .. Cell Culture In this study, two cancerous cell lines were used: T47D-KBluc human mammary ductal carcinoma cell line and A549 human pulmonary cancer cell line (American Type Culture Collection, Manassas, VA, USA). ..

Article Title: In vitro antiproliferative, anti-inflammatory effects and molecular docking studies of natural compounds isolated from Sarcocephalus pobeguinii (Hua ex Pobég)
Article Snippet: .. Cancerous cell lines (MCF-7: human breast adenocarcinoma cells; HepG2: human hepatocellular carcinoma cells; Caco-2: human epithelial colorectal adenocarcinoma cells; A549: human epithelial lung adenocarcinoma cells), obtained from the American Type Culture Collection (ATCC) (Rockville, MD, United States of America), were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM) high glucose (4.5 g/L) containing L-glutamine (4 mM) and sodium-pyruvate (HycloneTM) supplemented with 10% (v/v) fetal bovine serum (FBS) (Capricorn Scientific GmbH, South America), and incubated at 37°C with 5% CO 2 in a humidified environment. .. African green monkey (Vero) kidney cells (also obtained from ATCC), a non-cancerous cell line, were grown in DMEM high glucose (4.5 g/L) containing L-glutamine (Lonza, Belgium) and supplemented with 5% FBS (Capricorn Scientific GmbH, South America) and 1% gentamicin (Virbac, RSA) in the same environment as cancer cells.

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ACLY activity regulates MDR1 expression in colorectal cancer. (A) Transcript levels of ACLY and MDR1 (ABCB1) in colorectal cancer (red) and normal colon tissues (grey) analyzed using GEPIA (TCGA/GTEx datasets). (B) Immunoblot analysis of MDR1 in SW480 and DLD1 cells treated with the ACLY inhibitor BMS-303141 (20 or 50 μM, 48 h). (C) Immunoblot analysis of ACLY and MDR1 in SW480 and DLD1 cells transduced with empty vector (pLV) or ACLY-overexpressing vector (pLV[Exp]-hACLY). (D) Immunoblot analysis of ACLY and MDR1 in control and ACLY-overexpressing cells treated with BMS-303141 (50 μM, 48 h). (E) Relative ABCB1 mRNA levels in control and ACLY-overexpressing cells, and in cells treated with BMS-303141. (F) Relative ACLY mRNA levels under the same conditions. Data are presented as mean ± SD (n = 3 unless otherwise indicated). Statistical significance was determined using unpaired two-tailed t-tests or one-way ANOVA with Tukey’s post hoc test. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: Neoplasia (New York, N.Y.)

Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability

doi: 10.1016/j.neo.2026.101314

Figure Lengend Snippet: ACLY activity regulates MDR1 expression in colorectal cancer. (A) Transcript levels of ACLY and MDR1 (ABCB1) in colorectal cancer (red) and normal colon tissues (grey) analyzed using GEPIA (TCGA/GTEx datasets). (B) Immunoblot analysis of MDR1 in SW480 and DLD1 cells treated with the ACLY inhibitor BMS-303141 (20 or 50 μM, 48 h). (C) Immunoblot analysis of ACLY and MDR1 in SW480 and DLD1 cells transduced with empty vector (pLV) or ACLY-overexpressing vector (pLV[Exp]-hACLY). (D) Immunoblot analysis of ACLY and MDR1 in control and ACLY-overexpressing cells treated with BMS-303141 (50 μM, 48 h). (E) Relative ABCB1 mRNA levels in control and ACLY-overexpressing cells, and in cells treated with BMS-303141. (F) Relative ACLY mRNA levels under the same conditions. Data are presented as mean ± SD (n = 3 unless otherwise indicated). Statistical significance was determined using unpaired two-tailed t-tests or one-way ANOVA with Tukey’s post hoc test. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: Human colorectal cancer cell lines SW480 (KRASG12V) and DLD1 (KRASG13D) were obtained from the American Type Culture Collection (ATCC) and authenticated by short tandem repeat profiling.

Techniques: Activity Assay, Expressing, Western Blot, Transduction, Plasmid Preparation, Control, Two Tailed Test

ACLY activity modulates histone acetylation and MDR1 expression. (A) Immunoblot analysis of MDR1 in SW480 and DLD1 cells treated with the histone deacetylase inhibitor vorinostat (VOR; 0.5 μM for SW480 and 3.5 μM for DLD1) or DMSO for 24 h. Representative blots and densitometric quantification relative to control are shown. (B) Immunoblot analysis of acetylated histone H3 (H3K9ac) and histone H4 (H4K16ac) in SW480 wild-type (WT) and ACLY-overexpressing (OE) cells treated with vehicle or the ACLY inhibitor BMS-303141 (50 μM, 48 h). (C) Immunoblot analysis of H3K9ac and H4K16ac in DLD1 cells under the same conditions. β-actin was used as a loading control. Data are presented as mean ± SD (n = 3). Statistical significance was determined using unpaired two-tailed t-tests. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: Neoplasia (New York, N.Y.)

Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability

doi: 10.1016/j.neo.2026.101314

Figure Lengend Snippet: ACLY activity modulates histone acetylation and MDR1 expression. (A) Immunoblot analysis of MDR1 in SW480 and DLD1 cells treated with the histone deacetylase inhibitor vorinostat (VOR; 0.5 μM for SW480 and 3.5 μM for DLD1) or DMSO for 24 h. Representative blots and densitometric quantification relative to control are shown. (B) Immunoblot analysis of acetylated histone H3 (H3K9ac) and histone H4 (H4K16ac) in SW480 wild-type (WT) and ACLY-overexpressing (OE) cells treated with vehicle or the ACLY inhibitor BMS-303141 (50 μM, 48 h). (C) Immunoblot analysis of H3K9ac and H4K16ac in DLD1 cells under the same conditions. β-actin was used as a loading control. Data are presented as mean ± SD (n = 3). Statistical significance was determined using unpaired two-tailed t-tests. *P < 0.05; **P < 0.01; ***P < 0.001.

Techniques: Activity Assay, Expressing, Western Blot, Histone Deacetylase Assay, Control, Two Tailed Test

ACLY expression is associated with resistance-related transcriptional programs in colorectal cancer. (A) Correlation analysis between ACLY expression and a gene set associated with lipid metabolism (ACLY, ACSS2, ACSS1, FASN, SREBP1) and drug transport pathways (ABCB1, ABCC2, ABCG5, EpCAM, CD24) in colorectal cancer samples using GEPIA2 (TCGA dataset). (B) Schematic representation of a proposed model linking ACLY-dependent acetyl-CoA production to histone acetylation and transcriptional regulation in CRC cells. (C) Relative mRNA expression of EpCAM, ABCC2, and CD24 in SW480 and DLD1 cells overexpressing ACLY compared with empty vector controls. (D) Relative mRNA expression of EpCAM, ABCC2, and CD24 in SW480 and DLD1 cells treated with the ACLY inhibitor BMS-303141 (50 μM) compared with vehicle-treated controls. Gene expression levels were determined by qPCR and normalized to ACTB. Data are presented as mean ± SEM (n = 3). Statistical significance was determined using unpaired two-tailed t-tests. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: Neoplasia (New York, N.Y.)

Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability

doi: 10.1016/j.neo.2026.101314

Figure Lengend Snippet: ACLY expression is associated with resistance-related transcriptional programs in colorectal cancer. (A) Correlation analysis between ACLY expression and a gene set associated with lipid metabolism (ACLY, ACSS2, ACSS1, FASN, SREBP1) and drug transport pathways (ABCB1, ABCC2, ABCG5, EpCAM, CD24) in colorectal cancer samples using GEPIA2 (TCGA dataset). (B) Schematic representation of a proposed model linking ACLY-dependent acetyl-CoA production to histone acetylation and transcriptional regulation in CRC cells. (C) Relative mRNA expression of EpCAM, ABCC2, and CD24 in SW480 and DLD1 cells overexpressing ACLY compared with empty vector controls. (D) Relative mRNA expression of EpCAM, ABCC2, and CD24 in SW480 and DLD1 cells treated with the ACLY inhibitor BMS-303141 (50 μM) compared with vehicle-treated controls. Gene expression levels were determined by qPCR and normalized to ACTB. Data are presented as mean ± SEM (n = 3). Statistical significance was determined using unpaired two-tailed t-tests. *P < 0.05; **P < 0.01; ***P < 0.001.

Techniques: Expressing, Drug Transport Assay, Plasmid Preparation, Gene Expression, Two Tailed Test

Vitamin C induces coordinated changes in metabolic and chromatin-associated pathways in colorectal cancer cells. (A) Gene Ontology (GO) enrichment analysis of proteins differentially expressed following vitamin C treatment (5 mM, 4 h). (B) Volcano plot showing significantly upregulated and downregulated proteins (log₂ fold change > 1, p < 0.05). (C) KEGG pathway enrichment analysis highlighting pathways related to chromatin organization, DNA replication, nucleotide metabolism, and cell cycle regulation. (D) GO Cellular Component analysis showing enrichment of chromatin-associated complexes, including transcription regulator complexes, histone acetyltransferase-containing complexes, and Polycomb group (PcG) assemblies. (E) Heatmap representation of differentially expressed chromatin-associated proteins in control and vitamin C-treated cells. Proteomic analysis was performed in SW480 and DLD1 cells using label-free LC–MS/MS (diaPASEF). Data represent combined analysis of both cell lines.

Journal: Neoplasia (New York, N.Y.)

Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability

doi: 10.1016/j.neo.2026.101314

Figure Lengend Snippet: Vitamin C induces coordinated changes in metabolic and chromatin-associated pathways in colorectal cancer cells. (A) Gene Ontology (GO) enrichment analysis of proteins differentially expressed following vitamin C treatment (5 mM, 4 h). (B) Volcano plot showing significantly upregulated and downregulated proteins (log₂ fold change > 1, p < 0.05). (C) KEGG pathway enrichment analysis highlighting pathways related to chromatin organization, DNA replication, nucleotide metabolism, and cell cycle regulation. (D) GO Cellular Component analysis showing enrichment of chromatin-associated complexes, including transcription regulator complexes, histone acetyltransferase-containing complexes, and Polycomb group (PcG) assemblies. (E) Heatmap representation of differentially expressed chromatin-associated proteins in control and vitamin C-treated cells. Proteomic analysis was performed in SW480 and DLD1 cells using label-free LC–MS/MS (diaPASEF). Data represent combined analysis of both cell lines.

Techniques: Control, Liquid Chromatography with Mass Spectroscopy, Data-independent acquisition

Metabolic and epigenetic consequences of vitamin C treatment in colorectal cancer cells. (A) Quantification of ¹³C-glucose-derived citrate in SW480 and DLD1 cells treated with vitamin C (5 mM) for 4 h (n = 3). (B) Immunoblot analysis of total ACLY and phosphorylated ACLY at Ser455 following vitamin C treatment (5 mM) (n = 3). (C) Immunoblot analysis and quantification of acetylated histone H4 (AcH4K16) and histone H3 (AcH3K9) in SW480 and DLD1 cells after vitamin C exposure (n = 3). (D) MDR1 (ABCB1) protein levels in SW480 and DLD1 cells treated with vitamin C (5 mM), quantified relative to vehicle control (n = 3). (E) Relative ACLY and ABCB1 mRNA expression determined by qPCR after 6 h of vitamin C treatment (5 mM) in SW480 and DLD1 cells (n = 3). Data are presented as mean ± SEM. Statistical significance was determined using unpaired two-tailed t-tests. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: Neoplasia (New York, N.Y.)

Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability

doi: 10.1016/j.neo.2026.101314

Figure Lengend Snippet: Metabolic and epigenetic consequences of vitamin C treatment in colorectal cancer cells. (A) Quantification of ¹³C-glucose-derived citrate in SW480 and DLD1 cells treated with vitamin C (5 mM) for 4 h (n = 3). (B) Immunoblot analysis of total ACLY and phosphorylated ACLY at Ser455 following vitamin C treatment (5 mM) (n = 3). (C) Immunoblot analysis and quantification of acetylated histone H4 (AcH4K16) and histone H3 (AcH3K9) in SW480 and DLD1 cells after vitamin C exposure (n = 3). (D) MDR1 (ABCB1) protein levels in SW480 and DLD1 cells treated with vitamin C (5 mM), quantified relative to vehicle control (n = 3). (E) Relative ACLY and ABCB1 mRNA expression determined by qPCR after 6 h of vitamin C treatment (5 mM) in SW480 and DLD1 cells (n = 3). Data are presented as mean ± SEM. Statistical significance was determined using unpaired two-tailed t-tests. *P < 0.05; **P < 0.01; ***P < 0.001.

Techniques: Derivative Assay, Western Blot, Control, Expressing, Two Tailed Test

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human breast cancer cell line mcf 7 (ATCC)

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