Radiation resistance largely limits the survival of patients with non-small-cell lung cancer (NSCLC). To understand the mechanism underlying radiation resistance, we explored the influence of LINC01578 in radiation-resistant NSCLC cells. LINC01578, miR-216b-5p and Transducin (beta)-like 1 X-linked receptor 1 (TBL1XR1) expression was evaluated in patients with NSCLC, and their correlation with patients' prognosis was examined. Radiation-resistant NSCLC cell line (A549-RR) was induced and treated with oligonucleotide or plasmid transfection, and cell biological functions were captured. The interplay between LINC01578, miR-216b-5p and TBL1XR1 was clarified. NSCLC patients showed high LINC01578 and TBL1XR1 expression, and low miR-216b-5p expression, which was correlated to shorter patients' prognosis, respectively. LINC01578 or TBL1XR1 deficiency or miR-216b-5p elevation suppressed the functional activities of A549-RR cells. LINC01578 suppression elevated miR-216b-5p expression, consequently leading to the down-regulation of TBL1XR1. miR-216b-5p silencing or TBL1XR1 overexpression compromised LINC01578 knockdown's effects on radiation resistance of A549-RR cells. In brief, LINC01578 suppresses miR-216b-5p and enhances TBL1XR1 expression, thus to promote biological functions of radiation-resistant NSCLC cells.
Keywords: LINC01578; Non-small cell lung cancer; Transducin (beta)-like 1 X-linked receptor 1; biological function; radiation resistance.