Genome-wide CRISPR screen identifies MTA3 as an inducer of gemcitabine resistance in pancreatic ductal adenocarcinoma

Gemcitabine (GEM) resistance is one of the major causes of treatment failure in pancreatic ductal adenocarcinoma (PDAC) in clinic. Here, through CRISPR/Cas9 activation library screen, we found that MTA3 mediates the GEM resistance of PDAC and thus might be a potential therapeutic target for combinat...

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Veröffentlicht in:	Cancer letters 2022-11, Vol.548, p.215864-215864, Article 215864
Hauptverfasser:	Wu, Liangliang, Ge, Yi, Yuan, Yudong, Li, Hui, Sun, Huizhi, Xu, Chao, Wang, Yifei, Zhao, Tiansuo, Wang, Xiuchao, Liu, Jing, Gao, Song, Chang, Antao, Hao, Jihui, Huang, Chongbiao
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenocarcinoma Animals Antibodies Breast cancer Cancer therapies Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - metabolism Carrier Proteins - genetics Cell culture Cell Line, Tumor Chemoresistance Chemotherapy Cloning Colchicine CRISPR Deoxycytidine - analogs & derivatives Drug Resistance, Neoplasm - genetics Gemcitabine Gene silencing Genes Genomes Humans LIM Domain Proteins - genetics Medical prognosis Metastasis Mice Neoplasm Proteins - metabolism NF-kappa B - metabolism NF-κB protein Nucleosomes Pancreatic cancer Pancreatic Neoplasms Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Proteins Stat3 protein Therapeutic applications Therapeutic targets Tumor cells Xenograft Model Antitumor Assays Xenografts
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