Lung cancer is one of the most common malignant tumors and is currently the leading cause of cancer-related deaths worldwide. Although the treatment strategy has been significantly improved, the prognosis of lung cancer patients is still quite poor. RIOK1 has been reported to be highly expressed in non-small cell lung cancer (NSCLC), however, its clinical significance and biological function are still largely unknown in lung cancer. Using western blot and immunohistochemistry, we showed that RIOK1 was highly expressed in NSCLC tissues and correlated with advanced stage and poor prognosis. Furthermore, knockdown of RIOK1 could inhibit proliferation, migration, and invasion in NSCLC cells and tumorigenesis in vivo through AKT, Cyclin B1, MMP2, and EMT pathway. Furthermore, cell viability and apoptosis assays demonstrated that RIOK1 maintained NSCLC cell survival and reduced apoptosis rate when cells were treated with cisplatin. Western blot analysis demonstrated that RIOK1 depletion caused up-regulated protein expression of cleaved PARP and Caspase-3 in NSCLC cells. These findings revealed a novel function of RIOK1 in non-small cell lung cancer progression and suggest that RIOK1 might become a promising diagnostic and therapeutic target for this disease.
Keywords: RIOK1; chemical sensitivity; invasion; non-small cell lung cancer; proliferation.
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