Previous studies have demonstrated that NF-κB participates in the proliferation of lung cancer cells (Yu et al. Then, free active NF-κB (p65) translocates to the nucleus to regulate the transcriptional activity of antiapoptotic proteins (Bernal et al. After cytotoxic stimulation, IκB, which forms a complex with NF-κB, is phosphorylated and degraded by IκB kinase. The nuclear transcription factor κB (NF-κB) signalling pathway was confirmed to participate in the regulation of biological behaviours, including cell proliferation and apoptosis (Lawrence 2009 Peng et al. Hence, elucidation of the molecular mechanism of LUAD and identification of novel therapeutic targets are urgently needed. Over the past decade, rapid developments have been made in surgical removal, local ablation, vascular intervention and molecular targeted therapy for the treatment of lung cancer however, the 5-year survival rate remains low (Ettinger et al. Eighty-five per cent of lung cancer cases are non-small cell lung cancer (NSCLC), of which lung adenocarcinoma (LUAD) is the most common subtype (Herbst et al. Lung cancer is a common malignant neoplasm in China that seriously threatens the life and health of people. 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. Furthermore, blocking the NF-κB signalling pathway neutralized the effect of RTKN2 silencing in LUAD cells. RTKN2 overexpression increased p65 levels in the cytoplasm but decreased p65 levels in the nucleus. Additionally, p65 could be negatively regulated by RTKN2.
RTKN2 overexpression suppressed LUAD cell growth, invasion, migration, and glycolysis, while RTKN2 knockdown showed the opposite effects. RTKN2 levels were prominently decreased in LUAD tissues and cell lines. The p65 levels in the cytoplasm and nucleus were determined by western blot assays. RTKN2 expression was detected with qPCR, immunohistochemistry, and western blot assays. The interaction between RTKN2 and p65 was confirmed using a coimmunoprecipitation assay. The extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were evaluated by a Seahorse XFe96 analyser.
Transwell assays were carried out to assess cell migration and invasion. Cell proliferation was detected with CCK-8 and colony formation assays. The GEPIA online database was used to analyse abnormally expressed genes in lung adenocarcinoma and RTKN2 expression in various cancers.
This research was carried out to investigate the role of Rhotekin 2 (RTKN2) in LUAD progression. Lung adenocarcinoma (LUAD) is a malignant tumour that seriously threatens the life and health of people worldwide.
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