Published online Feb 14, 2021. doi: 10.3748/wjg.v27.i6.470
Peer-review started: October 20, 2020
First decision: December 8, 2020
Revised: December 21, 2020
Accepted: December 29, 2020
Article in press: December 29, 2020
Published online: February 14, 2021
Processing time: 108 Days and 8 Hours
Liver cancer is the sixth most common cancer in the world. Although miR-34a and palmitoyl membrane protein (MPP2) are reportedly involved in various cell processes, their precise roles in liver cancer are unknown.
miR-34a expression is low in liver cancer. The promoter region of miR-34a has CpG-binding sites and miR-34a is hypermethylated in liver cancer. MPP2 was downstream of miR-34a via miRDB and TargetScan databases prediction.
This study investigated the expression of miR-34a, the methylation of miR-34a promoter, and the expression of MPP2 in liver cancer cells and their related mechanisms.
The methylation degree of miR-34a promoter and the expression levels of miR-34a and MPP2 in the above samples were detected. miR-34a was demethylated by 5’-Za. miR-34a or MPP2 was upregulated by miR-34a mimics or MPP2 shRNA. The changes in proliferation, invasion, apoptosis, migration and other biological functions of liver cancer cells were observed. Double luciferase reporter genes were used to detect the targeting relationship between miR-34a and MPP2.
miR-34a and MPP2 were downregulated in liver cancer and miR-34a was highly methylated in liver cancer. After miR-34a demethylation/mimetic transfection/MPP2 overexpression, liver cancer cells apoptosis was increased, but the proliferation, invasion and migration capabilities were decreased. MPP2 was targeted by miR-34a.
miR-34a demethylation upregulates the expression of MPP2 in liver cancer cells and promotes the apoptosis of liver cancer cells.
The demethylation of miR-34a is a potential method for liver cancer treatment.