Objective: Increasing evidence suggested that dysregulated small nucleolar RNAs (snoRNAs) were involved in tumor development. The roles of snoRNA 71A (SNORA71A) in the progression of non-small cell lung cancer (NSCLC) remained unclear. Methods: Dataset GSE19188 from Gene Expression Omnibus (GEO) database was downloaded to detect the expression levels of SNORA71A in NSCLC tissues. The biological significance of SNORA71A was explored by loss-of-function analysis both in vitro and in vivo. Results: SNORA71A was overexpressed in NSCLC tissues compared with normal tissues, and upregulated SNORA71A was significantly associated with worse survival of NSCLC patients. Knockdown of SNORA71A suppressed proliferation of both A549 and PC9 cells, and induced G0/G1 phase arrest. Knockdown of SNORA71A also suppressed xenograft tumor growth in mice. In addition, knockdown of SNORA71A inhibited cell invasion and migration and suppressed epithelial-mesenchymal transition. Furthermore, downregulated SNORA71A decreased the phosphorylation of MEK and ERK1/2 in the MAPK/ERK signal pathway. Conclusion: SNORA71A functions as an oncogene in NSCLC and may serve as a therapeutic target and promising prognostic biomarker of NSCLC.
Keywords: MAPK/ERK; Non-small cell lung cancer; SNORA71A; Small nucleolar RNA; Tumorigenesis.