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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-142 inhibits lung cancer cell proliferation and promotes apoptosis by targeting XIAP
1Department of Integrated Chinese and Western Medicine, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, China. chuiguan092637296@yeah.net.
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.
Insights
MicroRNA-142 (miR-142) is downregulated in lung cancer, leading to increased X-linked inhibitor of apoptosis protein (XIAP). Restoring miR-142 inhibits lung cancer cell proliferation and promotes apoptosis by targeting XIAP.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- X-linked inhibitor of apoptosis protein (XIAP) is implicated in tumor development.
- Aberrant microRNA-142 (miR-142) expression is linked to lung cancer onset.
- Bioinformatics analysis suggests a regulatory relationship between miR-142 and XIAP.
Purpose of the Study:
- To investigate the role of miR-142 in regulating XIAP expression.
- To determine the effect of miR-142 on the biological processes of lung cancer cells.
Main Methods:
- Dual luciferase reporter gene assay to confirm miR-142 targeting of XIAP.
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to assess miR-142 and XIAP expression in lung cancer tissues and cell lines.
- EdU staining to analyze cell proliferation following miR-142 mimic transfection.
Main Results:
- miR-142 expression was significantly decreased, while XIAP expression was increased in lung cancer tissues compared to adjacent tissues.
- A direct targeting relationship between miR-142 and XIAP was confirmed.
- Overexpression of miR-142 in lung cancer cells inhibited XIAP expression, reduced cell proliferation, and promoted apoptosis.
Conclusions:
- Downregulation of miR-142 and upregulation of XIAP are associated with lung cancer development.
- miR-142 exerts tumor-suppressive effects in lung cancer by inhibiting XIAP expression, thereby reducing cell proliferation and inducing apoptosis.
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