RPS9 promotes the progression of NSCLC via activation Stat3 and Erk signaling pathways

Abstract

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.

Systematic analysis of various RNA transcripts and construction of biological regulatory networks at the post-transcriptional level for chronic obstructive pulmonary disease

“…*P < 0.05, **P < 0.01 p53, causing p53 to accumulate and inhibiting the proliferation of lung cancer cell lines [23]. Knockdown of RPS9 can significantly inhibit cell proliferation and metastasis and induce apoptosis in NSCLC through Stat3 and Erk signaling pathways [24]. Among these 18 COPD hub genes, only RPL32, RPL13A, and HSP90AA1 have been previously reported in COPD.…”

The interaction between the lemon ribosomal protein ClRPS9‐2 and citrus yellow vein clearing virus coat protein affects viral infection and gene silencing suppressor activity

“…RPS9 is a novel NPM1 interacting protein, that is one of the first proteins directly bound to 18S rRNA (Lindstrom & Zhang, 2008 ). RPS9 is involved in tumorigenesis and has a pro‐tumour role in osteosarcoma through activation of the mitogen‐activated protein kinase (MAPK) signalling pathway (Cheng et al, 2017 ; Iizumi et al, 2013 ; Kong et al, 2022 ). Moreover, evidence suggests that RPS9 plays a role in seed abortion, and embryo and endosperm development in maize and Arabidopsis thaliana (Lu et al, 2017 ; Ma & Dooner, 2004 ).…”

ACTN1 promotes malignant progression in Cutaneous Squamous Cell Carcinoma by reducing the p53 signaling pathway

“…Interestingly, previous studies have con rmed that RPL17 and RPS9 up-regulation were involved in non-small cell lung cancer, colorectal Cancer tumorigenesis by activating ERK, NEK2/b-catenin, and stat3 signaling pathways. [11][12] Therefore, the ACTN1 may be involved in the tumorigenic mechanisms of CSCC through a variety of biological pathways, and the p53 signaling pathway may be one important pathway according to KEGG enriched results combined with cluster B and C implications. Next, We focused on the ACTN1 and P53 interactions in CSCC.…”