RTKN2 Inhibits the Growth, Migration, Invasion and Glycolysis of Lung Adenocarcinoma Cells by Inactivating the NF-κB Signalling Pathway

Abstract

Abstract Background Lung adenocarcinoma (LUAD) is a malignant tumour that seriously threatens the life and health of people worldwide. This research was carried out to investigate the role of Rhotekin 2 (RTKN2) in LUAD progression. Methods and Results The GEPIA online database was used to analyse abnormally expressed genes in lung adenocarcinoma and RTKN2 expression in various cancers. Cell proliferation was detected with CCK-8 and colony formation assays. Transwell assays were carried out to assess cell migration and invasion. The extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were evaluated by a Seahorse XFe96 analyser. The interaction between RTKN2 and p65 was confirmed using a coimmunoprecipitation assay. RTKN2 expression was detected with qPCR, immunohistochemistry, and western blot assays. The p65 levels in the cytoplasm and nucleus were determined by western blot assays. RTKN2 levels were prominently decreased in LUAD tissues and cell lines. RTKN2 overexpression suppressed LUAD cell growth, invasion, migration, and glycolysis, while RTKN2 knockdown showed the opposite effects. Additionally, p65 could be negatively regulated by RTKN2. RTKN2 overexpression increased p65 levels in the cytoplasm but decreased p65 levels in the nucleus. Furthermore, blocking the NF-κB signalling pathway neutralized the effect of RTKN2 silencing in LUAD cells. Conclusion RTKN2 inhibited the malignant behaviour and glycolysis of LUAD cells by blocking the NF-κB signalling pathway, implying that RTKN2 could be a cancer suppressor in LUAD progression.