KIF22 promotes progress of esophageal squamous cell carcinoma cells and is negatively regulated by miR-122

Esophageal squamous cell carcinoma (ESCC) increases at fast rate of all cancer types in China, which urges the investigations of its potential mechanism. In this research, a highly expressed kinesin superfamily protein 22 (KIF22) was founded both in ESCC tissues and cancer cell lines. The following experiments pointed out that down-regulation of KIF22 remarkably restrained the malignant progression of ESCC cells. Besides, KIF22 knockdown promoted ESCC cells apoptosis and arrested cells in G0/G1 phase, while KIF22 also regulated the expression of cell cycle-and EMT-related proteins. Previous research revealed that the aberrant expressions of microRNAs (miRNAs) are related to tumors development. Based on the predict result, KIF22 was considered as the target of miR-122, which was demonstrated by luciferase reporter assay. miR-122 inhibitor could significantly reverse the function of KIF22 knockdown, including cell proliferation, migration and invasion. Furthermore, down expressed miR-122 altered the function of KIF22 knockdown on cell cycle-and EMT-related proteins. In a word, this work illustrated the regulatory function of KIF22/miR-122 axis in ESSC and provided potential targets for potential targets for ESSC treatment.

Automated summary

Esophageal squamous cell carcinoma (ESCC) shows a rapid increase in China, and the highly expressed KIF22 plays a crucial role in ESCC development. Down-regulation of KIF22 inhibits malignant progression of ESCC cells and promotes apoptosis, while also affecting cell cycle-and EMT-related proteins. MiR-122 is identified as a regulator of KIF22, providing a potential target for ESCC treatment.