lncRNA TINCR knockdown inhibits colon cancer cells via regulation of autophagy

Abstract

AbstractThe present study aimed to evaluate the effects of long noncoding (lnc)RNA TINCR ubiquitin domain containing (TINCR) on the development of colon cancer, and the specific underlying mechanisms. The present study used adjacent healthy and cancer tissues obtained from patients with colon cancer and measured lncRNA TINCR expression using reverse transcription‐quantitative (RT‐q) PCR and in situ hybridization assays. Moreover, associations between lncRNA TINCR and clinicopathology and prognosis were also investigated. In addition, the gene and protein expression levels of lncRNA TINCR, mTOR, LC 3B, P62, and Beclin1 were measured using RT‐qPCR and western blotting assays. Cell proliferation, apoptosis, invasion, and migration were measured using MTT, Edu staining, flow cytometry, TUNEL, Transwell, and wound‐healing assays, and cell ultrastructure and LC 3B activation were measured using transmission electron microscopy and cellular immunofluorescence. Results of the present study demonstrated that lncRNA TINCR expression was significantly upregulated in colon cancer tissues, and the overall survival of the low‐expression group was significantly increased, compared with that of the high‐expression groups. In addition, the results of the present study demonstrated that lncRNA TINCR was associated with clinicopathology in patients with colon cancer. Moreover, following lncRNA TINCR knockdown using transfection with small interfering RNA‐TINCR, results of the present study demonstrated that cell proliferation was significantly reduced, while cell apoptosis was significantly increased. In addition, cell invasion and migration were significantly reduced, and autophagy was increased in HT‐29 and SW620 cell lines. However, following treatment with an mTOR agonist (an autophagy inhibitor), biological activities were significantly increased in HT‐29 and SW‐620 cell lines. Collectively, these results demonstrated that lncRNA TINCR may induce colon cancer development through the regulation of autophagy.