acly inhibitor bms 303141 (MedChemExpress)
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acly inhibitor bms 303141
![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 <t>inhibitor</t> <t>BMS-303141</t> (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.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_2016/pmc13142016/pmc13142016__gr1.jpg)
Acly Inhibitor Bms 303141, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acly+inhibitor+bms+303141/BMS-303141/pmc13142016-38-1-4
Average 95 stars, based on 35 article reviews
Acly Inhibitor Bms 303141, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acly+inhibitor+bms+303141/BMS-303141/pmc13142016-38-1-4
Average 95 stars, based on 35 article reviews
acly inhibitor bms 303141 - by Bioz Stars,
2026-11
95/100 stars
Images
1) Product Images from "Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability"
Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability
Journal: Neoplasia (New York, N.Y.)
doi: 10.1016/j.neo.2026.101314
Figure Legend 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.
Techniques Used: Activity Assay, Expressing, Western Blot, Transduction, Plasmid Preparation, Control, Two Tailed Test
Figure Legend 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 Used: Activity Assay, Expressing, Western Blot, Histone Deacetylase Assay, Control, Two Tailed Test
Figure Legend 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 Used: Expressing, Drug Transport Assay, Plasmid Preparation, Gene Expression, Two Tailed Test
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