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MiR-142 inhibits lung cancer cell proliferation and promotes apoptosis by targeting XIAP.

Authors :
WU, X.-B.
LI, Q.-H.
ZHANG, N.
LI, M.
LI, K.
Source :
European Review for Medical & Pharmacological Sciences; 2019, Vol. 23 Issue 17, p7430-7437, 8p
Publication Year :
2019

Abstract

OBJECTIVE: The X-linked inhibitor of apoptosis protein (XIAP) is associated with the development of various tumors. The abnormal miR-142 expression is associated with the onset of lung cancer. Bioinformatics analysis revealed a targeted relationship between miR-142 and XIAP. This report investigated whether miR-142 plays a role in regulating XIAP expression and affecting the biological processes of lung cancer cells. PATIENTS AND METHODS: The tumor tissues of lung cancer patients were collected, and the adjacent tissues were used as controls. The dual luciferase reporter gene assay validated the targeted regulation between miR-142 and XIAP. Using BEAS-2B cells as control, qRT-PCR was used to detect the expression of miR-142 and XIAP in lung cancer cells A549 and H1650. Lung cancer H1650 cells were cultured and divided into miR-NC group and miR-142 mimic group followed by an analysis of cell proliferation by EdU staining. RESULTS: Compared with those in adjacent tissues, miR-142 expression was significantly decreased and XIAP expression was increased in lung cancer tissues. The Dual-Luciferase Reporter Assay confirmed a targeted regulation relationship between miR-142 and XIAP. Compared with BEAS-2B cells, miR-142 expression in lung cancer A549 and H1650 cells was significantly decreased, and XIAP expression was significantly increased. Transfection of miR-142 mimic significantly inhibited the expression of XIAP in H1650 cells, promoted apoptosis and inhibited cell proliferation. CONCLUSIONS: Decreased miR-142 expression and increased XIAP expression is associated with the onset of lung cancer. MiR-142 can inhibit lung cancer cell proliferation and induce apoptosis through inhibition of XIAP expression. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
11283602
Volume :
23
Issue :
17
Database :
Supplemental Index
Journal :
European Review for Medical & Pharmacological Sciences
Publication Type :
Academic Journal
Accession number :
138683506