Silencing linc00662 inhibits cell proliferation and colony formation of lung cancer cells via regulating the miR-145-5p-PAFAH1B2 axis.
Biochem Cell Biol
; 99(3): 330-338, 2021 06.
Article
em En
| MEDLINE
| ID: mdl-33108738
ABSTRACT
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.
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Base de dados:
MEDLINE
Assunto principal:
Biomarcadores Tumorais
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Regulação Neoplásica da Expressão Gênica
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MicroRNAs
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1-Alquil-2-acetilglicerofosfocolina Esterase
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RNA Longo não Codificante
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Neoplasias Pulmonares
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Proteínas Associadas aos Microtúbulos
Tipo de estudo:
Prognostic_studies
Limite:
Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Biochem Cell Biol
Assunto da revista:
BIOQUIMICA
Ano de publicação:
2021
Tipo de documento:
Article