BET inhibition decreases HMGCS2 and sensitizes resistant pancreatic tumors to gemcitabine

Efforts to develop targetable molecular bases for drug resistance for pancreatic ductal adenocarcinoma (PDAC) have been equivocally successful. Using RNA-seq and ingenuity pathway analysis we identified that the superpathway of cholesterol biosynthesis is upregulated in gemcitabine resistant (gemR)...

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Veröffentlicht in:	Cancer letters 2024-06, Vol.592, p.216919, Article 216919
Hauptverfasser:	Miller, Aubrey L., Fehling, Samuel C., Vance, Rebecca B., Chen, Dongquan, Brown, Eric Josh, Hossain, M. Iqbal, Heard, Eric O., Andrabi, Shaida A., Wang, Hengbin, Yang, Eddy S., Buchsbaum, Donald J., van Waardenburg, Robert C.A.M., Bellis, Susan L., Yoon, Karina J.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antimetabolites, Antineoplastic - pharmacology Azepines - pharmacology BET bromodomain inhibitor (BETi) Bromodomain Containing Proteins Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - metabolism Carcinoma, Pancreatic Ductal - pathology Cell Cycle Proteins - antagonists & inhibitors Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell Line, Tumor Deoxycytidine - analogs & derivatives Deoxycytidine - pharmacology Drug Resistance, Neoplasm - drug effects Female Gemcitabine Gemcitabine resistance (gemR) Gene Expression Regulation, Neoplastic - drug effects HMG-CoA synthase 2 (HMGCS2) Humans Hydroxymethylglutaryl-CoA Synthase - genetics Hydroxymethylglutaryl-CoA Synthase - metabolism Mice Mice, SCID Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Patient-derived xenograft (PDX) models Transcription Factors - antagonists & inhibitors Transcription Factors - genetics Transcription Factors - metabolism Triazoles - pharmacology Xenograft Model Antitumor Assays
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