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LncRNA KCNQ1OT1 promotes cell proliferation, migration and invasion via regulating miR-129-5p/JAG1 axis in non-small cell lung cancer.
Wang, Yan; Zhang, Lei; Yang, Jiasheng; Sun, Ruilin.
Afiliación
  • Wang Y; Department of Pulmonary and Critical Care Medicine, The Guangdong Second Provincial General Hospital, No. 466 Xingang Middle Rd, Haizhu District, 510000 Guangzhou, China.
  • Zhang L; 2Department of Transplant Centre, The Second Affiliated Hospital of Guangzhou Medical University, 510000 Guangzhou, China.
  • Yang J; Department of Pulmonary and Critical Care Medicine, The Guangdong Second Provincial General Hospital, No. 466 Xingang Middle Rd, Haizhu District, 510000 Guangzhou, China.
  • Sun R; Department of Pulmonary and Critical Care Medicine, The Guangdong Second Provincial General Hospital, No. 466 Xingang Middle Rd, Haizhu District, 510000 Guangzhou, China.
Cancer Cell Int ; 20: 144, 2020.
Article en En | MEDLINE | ID: mdl-32377169
ABSTRACT

BACKGROUND:

Non-small cell lung cancer (NSCLC) is the most deadly cancer worldwide. LncRNA KCNQ1OT1 has been reported to be involved in the progression of various tumors, including NSCLC. However, the precise mechanism of KCNQ1OT1 in NSCLC requires further investigation.

METHODS:

The expression levels of KCNQ1OT1, miR-129-5p and JAG1 were detected by qRT-PCR or western blot. Kaplan-Meier survival analysis was used to assess the correlation between KCNQ1OT1 expression and the overall survival of NSCLC patients. CCK-8 assay was used to measure cell viability. Cell migration and invasion were detected by transwell assay. The targets of KCNQ1OT1 and miR-129-5p were predicted by bioinformatics, which was confirmed by dual-luciferase reporter assay or pull-down assay.

RESULTS:

KCNQ1OT1 expression was significantly enhanced, while miR-129-5p expression was dramatically reduced in NSCLC tissues and cells. Higher KCNQ1OT1 shortened overall survival and was positively associated with tumor stage and lymph node metastasis. KCNQ1OT1 knockdown inhibited proliferation, migration and invasion of NSCLC cells. Inhibition of miR-129-5p attenuated the inhibition of NSCLC cell viability, migration and invasion induced by KCNQ1OT1 knockdown. In addition, JAG1 was confirmed as a target of miR-129-5p. Knockdown of JAG1 reversed the effects of miR-129-5p knockdown on NSCLC progression. KCNQ1OT1 regulated JAG1 expression by sponging miR-129-5p in NSCLC cells.

CONCLUSION:

KCNQ1OT1 induced proliferation, migration and invasion of NSCLC cells by sponging miR-129-5p and regulating JAG1 expression, indicating that KCNQ1OT1 was a therapeutic target for NSCLC.
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Cancer Cell Int Año: 2020 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Cancer Cell Int Año: 2020 Tipo del documento: Article País de afiliación: China