1. Department of Oncology, Huashan Hospital Fudan University, 12 Middle Urumqi Road, Shanghai 200040, China.
2. Department of Oncology, Shanghai Medical College Fudan University, Shanghai, 200032, China.
3. Department of Coronary Care Unit, The East Division of the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510700, China.
*These authors contributed equally to this work.
Background: Non-small cell lung cancer (NSCLC) accounts for the largest pathological type of lung cancers, and it is characterized by high incidence and poor prognosis. However, the molecular mechanisms involved in development and progression of NSCLC are not well elucidated. In this study, we aimed to explore the role and regulatory mechanism of RPS9 in NSCLC.
Materials and methods: The RPS9 expression in NSCLC tissues and cell lines was assessed by qRT-PCR and western blot. Knockdown of RPS9 induced by RNA interference (RNAi) method in PC9, A549 and H1299 cells. Overexpression of RPS9 induced by transient transfection in H292 cells. Cell proliferation, colony formation, metastasis and apoptosis abilities were determined by CCK-8 assay, colony formation assay, transwell assay and flow cytometry, respectively. The host signaling pathways affected by RPS9 were screened by antibody library and proved by western blot.
Results: RPS9 was significantly upregulated in NSCLC tissues and cell lines. Overexpression of RPS9 predicted poor prognosis of NSCLC patients. Knockdown of RPS9 obviously repressed cell proliferation, metastasis, and induced apoptosis. Mechanistically, suppression of RPS9 inhibited the expression level of phosphorylation of Stat3 and Erk.
Conclusion: Our study clarified that knockdown of RPS9 inhibits the progression of NSCLC via inactivation Stat3 and Erk signaling pathways.
Keywords: Non-small cell lung cancer, RPS9, progression, Stat3 and Erk signaling pathways