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MicroRNA-552 deficiency mediates 5-fluorouracil resistance by targeting SMAD2 signaling in DNA-mismatch-repair-deficient colorectal cancer.

Cancer Chemother. Pharmacol.. 2019; 
ZhaoPing,MaYu-Guang,ZhaoYang,LiuDi,DaiZhi-Jun,YanChang-You,GuanHai
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Mutagenesis Services The putative binding site of miR-552 in the three prime untranslated region (3′-UTR) of SMAD2 gene, along with its mutated derivative, was cloned into pGL3 Luciferase Reporter Vector (Promega, Shanghai, China), with the aid of CloneEZ® Kit (GenScript, HongKong, China) and QuikChange II Site-Directed Mutagenesis Kit (Agilent, Beijing China). Get A Quote

摘要

Although DNA-mismatch-repair-deficient (dMMR) status and aberrant expression of miRNAs are both critically implicated in the pathogenesis of resistance to 5-fluorouracil (5-FU) in colorectal cancer (CRC), whether these two factors regulate tumor response to 5-FU in a coordinated manner remains unknown. This study is designed to elucidate whether changes in miR-552 expression levels correlate to 5-FU-based chemoresistance in CRC, and to further identify the putative targets of miR-552 using multiple approaches.

关键词

5-Fluorouracil (5-FU),Chemoresistance,Colorectal cancer (CRC),TGF-β,m