LncRNA PCGEM1 accelerates non-small cell lung cancer progression via sponging miR-433-3p to upregulate WTAP.
BMC Pulm Med
; 20(1): 213, 2020 Aug 12.
Article
em En
| MEDLINE
| ID: mdl-32787827
ABSTRACT
BACKGROUND:
Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors all over the world. In recent years, long non-coding RNAs (lncRNAs) have been proven to participate in the development of different cancers, including NSCLC. PCGEM1 prostate-specific transcript (PCGEM1) is the lncRNA which is associated with the progression of several cancers. Nevertheless, in NSCLC, the specific functions of PCGEM1 are not yet clear.METHODS:
The real-time quantitative polymerase chain reaction (qPCR) was utilized to test the expression of PCGEM1 in NSCLC cells. Functional experiments, including cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, flow cytometry analysis and transwell assays were utilized to estimate cell proliferation, migration, invasion and apoptosis. Meanwhile, RNA pull down assay and luciferase reporter assay were utilized to evaluate the correlation of miR-433-3p with PCGEM1 or WT1 associated protein (WTAP).RESULT:
PCGEM1 was highly expressed in NSCLC cells, while miR-433-3p was lowly expressed in NSCLC cells. PCGEM1 silencing or miR-433-3p overexpression inhibited cell proliferation, migration and invasion but accelerated cell apoptosis. MiR-433-3p was proven be sponged by PCGEM1. Besides, WTAP was the target of miR-433-3p and it accelerated the progression of NSCLC. In the end, rescue experiments indicated that overexpression of WTAP or knockdown of miR-433-3p reversed the inhibited roles of silencing PCGEM1 on cell behavior.CONCLUSIONS:
PCGEM1 accelerates NSCLC progression via sponging miR-433-3p to upregulate WTAP.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Apoptose
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Carcinoma Pulmonar de Células não Pequenas
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Proteínas de Ciclo Celular
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MicroRNAs
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RNA Longo não Codificante
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Fatores de Processamento de RNA
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article