Silencing LncRNA LINC01305 inhibits epithelial mesenchymal transition in lung cancer cells by regulating TNXB-mediated PI3K/Akt signaling pathway.

Abstract

The aim of this study was to investigate whether LINC01305 can regulate TNXB-mediated phosphatidilinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway and therefore affect epithelial mesenchymal transition in lung cancer cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to detect LINC01305 level in 52 non-small cell lung cancer (NSCLC) tissues and paracancerous normal lung tissues, and the relationship between LINC01305 expression and clinical pathological parameters of these subjects was analyzed. After LINC01305 was knocked down in PC9 cell and overexpressed in A549 cells, qRT-PCR was used to verify the transfection efficiency, and nuclear fractionation technique, cell counting kit-8 (CCK-8), plate cloning assay and Transwell test were used to detect the effect of LINC01305 on cell viability. LINC01305 had an obviously higher expression in NSCLC tissues, and the expression in lung cancer patients with tumor size >3 cm was higher than those with tumor ≤3 cm. LINC01305 expression in tumor tissues in T3-T4 stage was obviously higher than those in T1-T2 stage, and the overall survival rate of lung cancer patients with high expression of LINC01305 was lower than those with low expression. Moreover, clinical analysis revealed that LINC01305 level was related to tumor size, TNM stage and lymph node metastasis of patients with lung cancer, but not related to age or gender. Silencing LINC01305 can inhibit the epithelial mesenchymal transition-induced transformation of lung cancer cells through regulating TNXB-mediated PI3K/Akt signaling pathway, which in turn affects the progression of lung cancer.