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 a common cancer and the main cause of cancer-related deaths worldwide. Liver cancer is the sixth most common cancer in the world. Although miR-34a and palmitoyl membrane palmitoylated protein (MPP2) are reportedly involved in various cell processes, their precise roles in liver cancer are still unclear.
To investigate the expression of micro RNA 34a (miR-34a), methylation of the miR-34a promoter and the expression of MPP2 in liver cancer cells and their related mechanisms.
Together, 78 cases of liver cancer tissues and 78 cases of adjacent tissues were collected. The methylation degree of miR-34a promoter in liver cancer/ paracancerous tissue and liver cancer cells/normal liver cells, and the expression levels of miR-34a and MPP2 in the above samples were detected. Demethylation of liver cancer cells or transfection of liver cancer cells with miR-34a mimetic was performed. The MPP2 overexpression vector was used to transfect liver cancer cells, and the changes in proliferation, invasion, apoptosis, migration, and other biological functions of liver cancer cells after the above interventions were observed. Double luciferase reporter genes were used to detect the targeting relationship between miR-34a and MPP2.
Clinical samples showed that the expression levels of miR-34a and MPP2 in liver cancer tissues were lower than those in the normal tissues. The methylation degree of miR-34a promoter region in liver cancer cells was higher than that in normal liver cells. After miR-34a demethylation/mimetic transfection/MPP2 overexpression, the apoptosis of liver cancer cells was increased; the proliferation, invasion and migration capabilities were decreased; the expression levels of caspase 3, caspase 9, E-cadherin, and B-cell lymphoma 2 (Bcl-2)-associated X protein were increased; and the expression levels of Bcl-2, N-cadherin, and β-catenin were decreased. Double luciferase reporter genes confirmed that MPP2 is targeted by miR-34a. Rescue experiments showed that small interfering MPP2 could counteract the promoting effect of miR-34a demethylation on apoptosis and the inhibitory effect on cell proliferation, invasion, and migration.
miR-34a demethylation upregulates the expression level of MPP2 in liver cancer cells and promotes the apoptosis of liver cancer cells. miR-34a demethylation is a potential method for liver cancer treatment.
Core Tip: This study confirmed the relationship of microRNA 34a (miR-34a) hypermethylation with membrane palmitoylated protein (MPP2) expression by investigating the changes of biological function and MPP2 expression level of liver cancer cells after miR-34a demethylation. miR-34a can inhibit the occurrence of liver cancer by upregulating MPP2, and its demethylation in liver cancer cells is a potential method of liver cancer treatment. In essence, miR-34a methylation is located upstream of its binding site with p53. Therefore, it is valuable to study the role of miR-34a methylation/demethylation on the expression level of upstream regulatory factors such as p53, and to explore its function in the future.