Published online Oct 15, 2019. doi: 10.4251/wjgo.v11.i10.842
Peer-review started: May 7, 2019
First decision: June 4, 2019
Revised: June 19, 2019
Accepted: July 26, 2019
Article in press: July 28, 2019
Published online: October 15, 2019
Processing time: 176 Days and 22.2 Hours
Ectopic expression of miRNAs promotes tumor development and progression. miRNA (miR)-320a is downregulated in many cancers, including gastric cancer (GC). However, the mechanism underlying its downregulation and the role of miR-320a in GC are unknown.
To determine expression and biological functions of miR-320a in GC and investigate the underlying molecular mechanisms.
Quantitative real-time polymerase chain reaction (PCR) was used to determine expression of miR-320a in GC cell lines and tissues. TargetScanHuman7.1, miRDB, and microRNA.org were used to predict the possible targets of miR-320a, and a dual luciferase assay was used to confirm the findings. Western blotting was used to detect the protein levels of pre-B-cell leukemia homeobox 3 (PBX3) in GC cells and tissue samples. Cell Counting Kit-8 proliferation, Transwell, wound healing, and apoptosis assays were performed to analyze the biological functions of miR-320a in GC cells. Methylation-specific PCR was used to analyze the methylation level of the miR-320a promoter CpG islands. 5-Aza-2’-deoxycytidine (5-Aza-CdR) and trichostatin A (TSA) were used to treat GC cells.
miR-320a expression was lower in GC cell lines and tissues than in the normal gastric mucosa cell line GES-1 and matched adjacent normal tissues. miR-320a overexpression suppressed GC cell proliferation, invasion and migration, and induced apoptosis. PBX3 was a target of miR-320a in GC. The methylation level of the miR-320a promoter CpG islands was elevated and this was partly reversed by 5-Aza-CdR and TSA.
miR-320a acts as a tumor suppressor and inhibits malignant behavior of GC cells, partly by targeting PBX3. DNA methylation is an important mechanism associated with low expression of miR-320a.
Core tip: miRNA (miR)-320a functioned as a tumor suppressor and was downregulated in gastric cancer (GC). miR-320a overexpression suppressed proliferation, migration and invasion, and induced apoptosis through targeting Pre-B-cell leukemia homeobox 3 in GC cells. miR-320a depletion showed the opposite results. The potential mechanism of miR-320a deficiency in GC was the increased methylation level of the miR-320a promoter CpG islands.