LncRNA TNK2-AS1/miR-125a-5p axis promotes tumor growth and modulated PI3K/AKT pathway.

Abstract

BACKGROUND\nLong non-coding RNA (lncRNA) TNK2 AS1 is a noncoding RNA with the capability of affecting MicroRNAs (miRNAs)levels and gene expression.\n\n\nOBJECTIVES\nThe study was designed to investigate the mechanism of TNK2 AS1 in gastric cancer.\n\n\nMETHODS\nThe loss and gain of function of TNK2 AS1 was investigated by analyzing the malignant behavior of AGS cells including the abilities of migration, invasion and epithelial-mesenchymal transition (EMT) process via Wound healing and Transwell assay, as well as Western blot. The targeting relationship of LncRNA TNK2 AS1 was analyzed through searching bioinformatics database, Luciferase Reporter Assay and RNA immunoprecipitation (RIP) assay. Tumor-bearing experiment in nude mice was performed to further confirm the regulatory role of TNK2 AS1 in vivo. Immunofluorescence assay for Ki67 expression was carried out in tumor tissues of mice model.\n\n\nRESULTS\nThe results showed that TNK2 AS1 overexpression promoted the malignant behaviors of AGS cells, which could be weakened by miR-125a-5p mimic addition. In addition, Jumonji, At-rich Interaction Domain (JARID2) and phosphatidylinositol 3 kinase (PI3K)/AKT pathway were regulated by TNK2-AS1/miR-125a-5p axis. In vivo, TNK2 AS1/miR-125a-5p axis promoted tumor growth and led to increases in green fluorescence intensity, Vimentin expression and a decrease in E-cadhein level, which could be mediated by JARID2 and PI3K/AKT pathway.\n\n\nCONCLUSION\nTherefore, a conclusion was drawn that TNK2-AS1/miR-125a-5p promoted the progression of gastric cancer.