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Published on: March 30, 2019
linc00511 Knockdown Inhibits Lung Cancer Progression by Regulating miR-16-5p/MMP11
Zhengyi Song1, Jing Luo1, Ming Wu2
1Chest Surgery, National Medicine Gezhouba Central Hospital, Yichang 443000, Hubei, China.
Abstract:
Lung cancer (LC) is a malignant tumor that extremely impairs people. According to numerous studies, long non-coding RNA (lncRNA) was inextricably involved in the advancement of LC. The work aspired to identify linc00511 expression in LC and to dig for the underlying mechanisms linc00511 regulated LC progression. Experimental outcomes revealed that linc00511 was obviously upregulated in LC, and linc00511 knockdown significantly impaired the malignant phenotype of LC cells in vitro. For an in-depth study on the contribution of linc00511 to LC advancement, it was disclosed that miR-16-5p had binding sites to the sequence of linc00511, which also inversely affected linc00511 expression in LC. Further experimental data demonstrated that miR-16-5p directly and negatively targeted matrix metallopeptidase 11 (MMP11). Also, rescue experiments displayed that miR-16-5p inhibition or MMP11 overexpressing offset the suppressive impacts of linc00511 silencing on LC progression. To sum up, our findings indicated that linc00511 performed a crucial role in facilitating LC progression, and mechanistic studies demonstrated that linc00511 aggravated LC progression via targeting the miR-16-5p/MMP11 axis.
Insights
Long non-coding RNA linc00511 promotes lung cancer (LC) progression by targeting the miR-16-5p/MMP11 axis. Silencing linc00511 inhibits LC cell malignancy, offering potential therapeutic targets.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Lung cancer (LC) is a major global health concern.
- Long non-coding RNAs (lncRNAs) are implicated in LC development.
- The specific role of linc00511 in LC remains to be fully elucidated.
Purpose of the Study:
- To investigate the expression and function of linc00511 in lung cancer.
- To explore the underlying molecular mechanisms by which linc00511 influences LC progression.
- To identify potential therapeutic targets within the linc00511 regulatory pathway.
Main Methods:
- Quantitative real-time PCR to assess linc00511 expression in LC tissues and cells.
- In vitro assays (e.g., cell proliferation, migration, invasion) to evaluate the functional impact of linc00511.
- Bioinformatic analysis and luciferase reporter assays to confirm interactions between linc00511, miR-16-5p, and MMP11.
- Rescue experiments to validate the role of the miR-16-5p/MMP11 axis in linc00511-mediated LC progression.
Main Results:
- Linc00511 expression was significantly upregulated in lung cancer tissues and cells.
- Knockdown of linc00511 suppressed the proliferation, migration, and invasion of LC cells in vitro.
- Linc00511 directly interacted with miR-16-5p, and miR-16-5p was found to target MMP11.
- Inhibition of miR-16-5p or overexpression of MMP11 reversed the suppressive effects of linc00511 silencing on LC progression.
Conclusions:
- Linc00511 acts as a crucial oncogenic lncRNA in lung cancer.
- Linc00511 promotes LC progression by sponging miR-16-5p, leading to increased MMP11 expression.
- The linc00511/miR-16-5p/MMP11 axis represents a potential therapeutic target for lung cancer treatment.
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