miR-139-5p mediates TGIF1 to regulate the TGFβ pathway and inhibit growth of esophageal squamous cell carcinoma cells

Abstract

Background

Esophageal squamous cell carcinoma (ESCC) is the most prevalent histological subtype of esophageal cancer. miR-139-5p has been shown to have abnormal expression in ESCC. We intend to probe into the roles of miR-139-5p in ESCC, thus providing references for investigating underlying therapeutic targets.

Methods

miR-139-5p expression in esophageal carcinoma was predicted by the Starbase online website. miR-139-5p expression in human ESCC cell lines (KYSE-150, KYSE-410, KSE-30) and human esophageal epithelial cell line Het1A was determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR). KYSE-150 cells were manipulated with miR-139-5p mimic to upregulate miR-139-5p. Cell colony formation, viability, apoptosis, migration, and invasion were assessed by colony formation assay, CCK‑8, flow cytometry, wound healing test, and Transwell. The targeted binding between miR-139-5p and TGIF1 was predicted on Starbase, Targetscan, and miRDB online websites and verified by Dual-Luciferase assay. Cells were transfected with miR-139-5p mimic and pcDNA3.1 TGIF1. The phosphorylation levels of TGFβ pathway-related proteins Smad2 and Smad3 were assessed by RT-qPCR and western blot.

Results

miR-139-5p was underexpressed in ESCC cells. miR-139-5p overexpression reduced ESCC cell viability, migration, and invasion, and promoted apoptosis. TGIF1 overexpression averted miR-139-5p mimic-inhibited ESCC cell growth. miR-139-5p overexpression decreased the phosphorylation levels of TGFβ pathway-related proteins Smad2 and Smad3, while the phosphorylation levels were increased by additional TGIF1 vector transfection.

Conclusion

miR-139-5p mediates TGIF1 to regulate TGFβ pathway and inhibit ESCC cell growth.