Bioinformatic analysis of miR-4792 regulates Radix Tetrastigma hemsleyani flavone to inhibit proliferation, invasion, and induce apoptosis of A549 cells.

ABSTRACT:

Background

Radix Tetrastigma hemsleyani, a kind of Chinese medicinal herb, contains multiple medicinal ingredients and can exert a variety of pharmacological activities. Our previous study revealed that miR-4792 was significantly upregulated in Radix Tetrastigma hemsleyani flavone (RTHF)-treated A549 cells; however, the regulatory mechanism of RTHF-treated A549 cells remains unclear.

Materials and methods

In this study, we investigated the antitumor mechanism and regulatory pathway of miR-4792 in RTHF-treated A549 cells, and the target genes were predicted and pathway enrichment of miR-4792 was performed using bioinformatic analysis.

Results

Our results confirmed that the upregulated expression of miR-4792 could inhibit cell proliferation and invasion, provoke cell cycle arrest, and induce apoptosis in A549 cells. Gene Ontology analysis showed that target genes of miR-4792 were enriched in protein binding, cytosol, cytoplasm, plasma membrane, and metal ion binding. Kyoto Encyclopedia of Genes and Genomes analysis showed that target genes of miR-4792 were enriched in aminoacyltRNA biosynthesis, AGE-RAGE signaling pathway in diabetic complications, sphingolipid signaling pathway, neuroactive ligand-receptor interaction, glycosaminoglycan degradation, and regulation of lipolysis in adipocytes. Additionally, FOXC1 was identified as an important target gene of miR-4792 in RTHF-treated A549 cells, and miR-4792 may be the target of some apoptotic-related proteins involved in induction of apoptosis in A549 cells by RTHF. Moreover, the intracellular Ca²⁺ levels of A549 cells were increased after RTHF treatment, which may be involved in the anticancer regulatory process of miR-4792 in RTHF-treated A549 cells.

Conclusion

These findings suggest a novel therapeutic approach for lung cancer that will be investigated in future studies.

SUBMITTER: Liu P 

PROVIDER: S-EPMC6389004 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature