Silencing linc00662 inhibits cell proliferation and colony formation of lung cancer cells via regulating the miR-145-5p–PAFAH1B2 axis
Autor: | Hong-Zhong Cheng, Jun Peng, Yang Wang, Han Wang, Guo-Ping Wang, Zheyuan Xu, Zhi-Zhou Shi, Xin-Long Chen, Hao Peng, Wen Jiang |
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Rok vydání: | 2021 |
Předmět: |
Male
0301 basic medicine Lung Neoplasms Apoptosis Biology Biochemistry 03 medical and health sciences 0302 clinical medicine microRNA Biomarkers Tumor Tumor Cells Cultured medicine Humans Gene silencing Lung cancer Molecular Biology Aged Cell Proliferation Gene knockdown Oncogene Competing endogenous RNA Cell growth Cell Biology Middle Aged respiratory system Prognosis medicine.disease respiratory tract diseases Gene Expression Regulation Neoplastic Survival Rate MicroRNAs 030104 developmental biology 030220 oncology & carcinogenesis 1-Alkyl-2-acetylglycerophosphocholine Esterase Cancer research Adenocarcinoma Female RNA Long Noncoding Microtubule-Associated Proteins |
Zdroj: | Biochemistry and Cell Biology. 99:330-338 |
ISSN: | 1208-6002 0829-8211 |
Popis: | Lung cancer is the most common cause of cancer-related death in the world. Long non-coding RNAs (lncRNAs) are longer than 200 nucleotide transcripts, and are not translated into protein. The lncRNA linc00662 is overexpressed in lung cancer; however, its role in lung cancer is still unknown. In our study, by analyzing the TCGA data, we found that linc00662 was overexpressed in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). We knocked-down the expression of linc00662 using siRNA, and found that silencing linc00662 significantly inhibited the proliferation and colony formation of the lung cancer cell lines A549 and H460. We also found that knockdown of linc00662 increased the expression of the microRNA miR-145-5p and decreased the expression of the platelet-activating factor acetylhydrolase IB subunit beta (PAFAH1B2) gene. We further show that linc00662 binds with miR-145-5p, and that miR-145-5p binds to the 3′UTR of PAFAH1B2. miR-145-5p negatively regulates PAFAH1B2 both at the mRNA and the protein level. Loss of miR-145-5p abolished the inhibitory effects of silencing linc00662 on the proliferation and colony formation of A549 and H460 cells. These findings indicate that linc00662 functions as an oncogene by acting as a competing endogenous RNA (ceRNA) and sponges and regulates miR-145-5p in lung cancer, and thus may provide a potential target for treating lung cancer. |
Databáze: | OpenAIRE |
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