The aim of the present study was to examine the function of unc-51 like autophagy activating
kinase 2 (Ulk2) in
non-small cell lung cancer (NSCLC). Western blotting was used to analyze the
protein expression of Ulk2 in seven pairs of cancerous and adjacent non-cancerous NSCLC specimens. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis was used to determine the
mRNA expression of Ulk2 in 20 pairs of
tumor and adjacent normal tissues. Two NSCLC cell lines, A549 and H460, were transfected with an Ulk2 overexpression plasmid or empty vector; cell proliferation and chemosensitivity were measured using an MTT assay, and flow cytometry and western blotting were used to evaluate apoptosis. A nude mouse
tumorigenesis experiment was used to assess
tumor volume in vivo, using A549 cells stably overexpressing Ulk2 and control cells. The
protein expression levels of Ulk2 were significantly lower in 6/7 (85.7%) cases of NSCLC compared with in non-cancerous tissues, as determined by western blotting (P<0.05). The
mRNA expression levels of Ulk2 were significantly lower in 16/20 (70.0%) NSCLC specimens compared with in non-cancerous tissues, as revealed by RT-qPCR (P<0.05). Overexpression of Ulk2 significantly inhibited the proliferation of A549 and H460 cells (P<0.05) and sensitized the NSCLC cell lines to
cisplatin- and
etoposide-induced inhibition of proliferation, and to
cisplatin-induced apoptosis, with a significant difference identified compared with the control group (P<0.05). Overexpression of Ulk2 significantly increased basal autophagy levels in A549 and H460 cells (P<0.05). Thus, Ulk2-induced enhanced chemosensitivity was suggested to be partly mediated through increased autophagy. The overexpression of Ulk2 significantly suppressed
tumor volume in vivo (P<0.05). Overexpression of Ulk2 inhibits
cancer cell proliferation and enhances chemosensitivity to
cisplatin in NSCLC.