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LINC01303 promotes the proliferation and migration of laryngeal carcinoma by regulating miR-200c/TIMP2 axis.

ABSTRACT:

Background

It is reported that long non-coding RNA is crucial in many cancer progressions. But the function and regulatory mechanism of LINC01303 in human laryngeal squamous cell carcinoma (LSCC) remains unclear. Hence, this research aims at investigating the biological function and potential mechanism of LINC01303 in LSCC.

Methods

Real-time quantitative PCR (qRT-PCR) was applied for the determination of LINC01303, miR-200c and TIMP metallopeptidase inhibitor 2 (TIMP2) expression in LSCC tissues and cell lines. Corresponding experiments were carried out to determine the impacts of LINC01303 on LSCC cell proliferation, apoptosis, migration and invasion. The interaction between LINC01303 and miR-200c was analyzed with bioinformatics analysis and luciferase activity analysis.

Results

LINC01303 expression in LSCC tissues was notably higher than that in adjacent normal tissues. High LINC01303 expression was bound up with lymphatic metastasis and advanced clinical stage. In addition, inhibition of LINC01303 by siRNA could evidently block LSCC cell proliferation, induce apoptosis, and inhibit invasion and migration. Mechanically, LINC01303 acted as carcinogenic lncRNA in LSCC by regulating miR-200c/TIMP2 axis.

Conclusion

LINC01303 plays a carcinogenic part in LSCC carcinogenesis through regulating miR-200c/TIMP2 axis, which may become a promising target of LSCC therapy.

SUBMITTER: Xiao D

PROVIDER: S-EPMC8014399 | biostudies-literature |

REPOSITORIES: biostudies-literature

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