Regulatory effect of Nemo-like kinase on nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is the leading malignant tumor in ear-nose-throat. It has high incidence in China with regional distribution. Multiple factors underlie the pathogenesis of NPS. Nemo-like kinase (NLK) is one novel tumor marker identified recently and exerts pro-or anti-tumor functions. Previous study has indicated up-regulation of NLK in NPC, but with unclear mechanism so far. Cultured CNE2 cells were transfected with small interference RNA (siRNA) of NLK. Real-time PCR and Western blotting described the expressional profile of NLK in cells. The proliferation was quantified by MTT assay, while the invasion ability was determined by Transwell chamber invasion assay. Further studies tested caspase-3 activity and expression of Bcl-2 and Bax proteins in CNE2 cells. SiRNA transfection significantly depressed mRNA and protein levels of NLK compared to scramble RNA group (P<0.05). Such down-regulation of NLK inhibited proliferation of CNE2 cells and depressed tumor invasion. In those NLK-knock down cells, caspase-3 activity was potentiated, along with lower Bcl-2 protein and higher Bax protein levels (P<0.05). Down-regulating NLK in NPC cells can facilitate tumor cell apoptosis, and inhibit the survival and progression of tumors.