Open Accesshsa_circ_0058357 acts as a ceRNA to promote non‑small cell lung cancer progression via the hsa‑miR‑24‑3p/AVL9 axis
Author(s) -
Dong Wei,
Lifang Sun,
Wei Feng
Publication year - 2021
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2021.12109
Subject(s) - gene knockdown , competing endogenous rna , cell growth , apoptosis , cancer research , microrna , biology , cell cycle , flow cytometry , oncogene , cell , cell migration , cancer cell , cancer , microbiology and biotechnology , rna , gene , biochemistry , genetics , long non coding rna
Abnormal circular RNAs (circRNAs) are associated with biological processes in cancer; however, the function of circRNAs remains largely unknown in non‑small cell lung cancer (NSCLC). The present study aimed to investigate the role of hsa_circ_0058357 on the progression of NSCLC. Cell proliferation, migration and apoptosis were determined using Cell Counting Kit‑8, Transwell and flow cytometry assays, respectively. Gene [circRNA and microRNA (miR)] and protein expression levels were determined via reverse transcription‑quantitative PCR and immunoblotting. A luciferase assay was employed to detect the binding of miR‑24‑3p with AVL9 cell migration associated ( AVL9 ), while a cancer xenograft model was established to evaluate cancer growth in vivo . The results demonstrated that hsa_circ_0058357 was highly expressed in human NSCLC tissues and NSCLC cells compared with para‑cancerous tissues and human bronchial epithelial (HBE) cells, respectively. Knockdown of hsa_circ_0058357 significantly suppressed cell viability, migration and tumor growth, while it promoted apoptosis in NSCLC cells. As a competing endogenous RNA, hsa_circ_0058357 knockdown contributed to the increase of miR‑24‑3p expression in NSCLC cells. Of note, overexpression of miR‑24‑3p markedly abolished the exogenous hsa_circ_0058357‑induced excessive proliferation, migration and apoptosis resistance of NSCLC cells. Mechanistically, as a signaling molecule in late secretory pathway, AVL9 was also expressed at a high level in NSCLC tissues and cells, which could be directly suppressed by miR‑24‑3p. In the tumor tissues, along with growth inhibition, hsa_circ_0058357 knockdown also mediated the elevation of miR‑24‑3p and the reduction of AVL9. Thus, it was suggested that hsa_circ_0058357 may be a crucial regulation factor in NSCLC by sponging hsa‑miR‑24‑3p, leading to a decrease in miR‑24‑3p expression, and subsequent increase in AVL9 expression. Therefore, hsa_circ_0058357 may serve as a potential target for diagnosis and gene therapy for NSCLC.