Background
PLIN5 is abnormally expressed in many forms of tumors, but its activity and methylation status in human ovarian cancer (OC) have yet to be elucidated.
Conclusions
Our findings suggest that the expression level of PLIN5 is regulated by methylation, and in OC, PLIN5 can act as a tumor suppressor.
Methods
RNA sequencing data (RNA-seq) were downloaded from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) database. Differentially expressed genes (DEGs) were identified, and then PLIN5 gene was selected for further study. Expression and methylation levels of PLIN5 were detected by qPCR, western blot, immunohistochemical, and MSP analysis. Moreover, colony formation, transwell, and cell apoptosis assays were employed to explore the abilities of cell proliferation, migration, invasion, and apoptosis, respectively. Furthermore, PLIN5's function on tumorigenesis was determined by in vivo experiments.
Results
We found that PLIN5 was downregulated in OC tissues by using qPCR, western blot, and immunohistochemical analyses, and MSP also exhibited that PLIN5 was hypermethylated in OC tissues. The expression level of PLIN5 could be restored after treatment with 5-Aza-dC. Furthermore, we found that demethylated PLIN5 could suppress cell proliferation, migration, and invasion of OC, and increase cell apoptosis. Moreover, xenograft experiments showed that demethylated PLIN5 could suppress tumor growth. Conclusions: Our findings suggest that the expression level of PLIN5 is regulated by methylation, and in OC, PLIN5 can act as a tumor suppressor.