期刊
BIOENGINEERED
卷 12, 期 1, 页码 4044-4053出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2021.1951930
关键词
Mir-506-3p; colorectal cancer; enhancer of zeste homologue 2 (ezh2)
The study found that miR-506-3p inhibited the progression of CRC by targeting EZH2 expression, providing a new molecular target for the clinical treatment of CRC in the future.
A large number of studies have shown that microRNA (miRNA) has an important relationship with the occurrence and development of colorectal cancer (CRC), but its specific molecular mechanism has not been fully elucidated. This study is to explore the influence of miR-506-3p on the malignant behavior of CRC and its underlying molecular mechanism. Our results show that miR506-3p was lowly expressed and enhancer of zeste homologue 2 (EZH2) was highly expressed in CRC. Overexpressing miR-506-3p or silencing EZH2 inhibited CRC cell proliferation, migration and invasion and promoted apoptosis. Inhibiting miR-506-3p promoted CRC cell proliferation, migration and invasion but inhibited apoptosis. These impacts were reversed after co-transfecting siEZH2. Further mechanism studies have shown that miR-506-3p can reduce EZH2 expression in CRC cells by binding to the 3'UTR end of EZH2. In summary, the results of this study show that miR-506-3p inhibited CRC progression through targeting EZH2 expression. This provides a new molecular target for the clinical treatment of CRC in the future. [GRAPHICS]
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