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LINC-PINT alleviates lung cancer progression via sponging miR-543 and inducing PTEN
Shu Wang1, Wenyang Jiang2, Xinghua Zhang2
1Department of Gerontology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Abstract:
Long intergenic nonprotein coding RNA p53-induced transcript (LINC-PINT) has been reported to participate in various cancers. Here, we investigated the effects of LINC-PINT on lung cancer progression. Firstly, in our study, we implied that LINC-PINT was obviously decreased in NSCLC. Thereafter, in A549 and H1299 cells, LINC-PINT was upregulated via transfecting LV-LINC-PINT. As exhibited, LINC-PINT repressed cell proliferation and cell colony formation of A549 and H1299 cells. Subsequently, flow cytometry evidenced that A549 and H1299 cell apoptosis was obviously triggered and the cell cycle was arrested in G1 phase. Then, migration and transwell invasion experiments were carried out to detect the cell migration and invasion capacity. We found A549 and H1299 cell migration and invasion capacity were restrained by the upregulation of LINC-PINT. Meanwhile, we predicted that miR-543 could function as the target of LINC-PINT and the association was verified. Moreover, we exhibited that miR-543 was remarkably increased in lung cancer, which could be regulated by LINC-PINT negatively. Furthermore, PTEN could act as the downstream target of miR-543 and upregulation of miR-543 repressed PTEN, which was reversed by LV-PINT in A549 and H1299 cells. Finally, xenografts were utilized to confirm the function of LINC-PINT on lung cancer. All these findings concluded that LINC-PINT exerted crucial biological roles in NSCLC through sponging miR-543 and inducing PTEN.
Insights
Long intergenic nonprotein coding RNA p53-induced transcript (LINC-PINT) is decreased in non-small cell lung cancer (NSCLC). Upregulating LINC-PINT inhibits NSCLC cell proliferation, migration, and invasion by targeting miR-543 and PTEN.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long intergenic nonprotein coding RNA p53-induced transcript (LINC-PINT) is implicated in various cancers.
- The role of LINC-PINT in non-small cell lung cancer (NSCLC) progression requires further investigation.
Purpose of the Study:
- To investigate the functional role of LINC-PINT in NSCLC progression.
- To elucidate the molecular mechanism underlying LINC-PINT's action in lung cancer.
Main Methods:
- Quantitative analysis of LINC-PINT expression in NSCLC tissues and cell lines.
- In vitro experiments involving LINC-PINT upregulation in A549 and H1299 cells (proliferation, colony formation, apoptosis, cell cycle, migration, invasion assays).
- In vivo xenograft models and molecular mechanism studies (miRNA target prediction and validation, Western blotting for protein expression).
Main Results:
- LINC-PINT expression was significantly decreased in NSCLC.
- Overexpression of LINC-PINT suppressed NSCLC cell proliferation, colony formation, migration, and invasion.
- LINC-PINT upregulation induced apoptosis and G1 phase cell cycle arrest.
- LINC-PINT negatively regulated miR-543, and miR-543 targeted PTEN, inhibiting its expression.
- LINC-PINT overexpression reversed the inhibitory effect of miR-543 on PTEN.
Conclusions:
- LINC-PINT plays a critical role in suppressing NSCLC progression.
- LINC-PINT acts as a tumor suppressor in NSCLC by sponging miR-543 and upregulating PTEN.
- LINC-PINT represents a potential therapeutic target for NSCLC treatment.
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