linc00511 Knockdown Inhibits Lung Cancer Progression by Regulating miR-16-5p/MMP11

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 <i>in vitro</i>. 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.

MMP11 as a prognostic biomarker correlated with immune infiltrates in pancreatic adenocarcinoma

“…Our findings showed that MMP11 was overexpressed in many cancers and was associated with a poor prognosis. Previous research has shown that the downregulation of MMP11 expression reduced the growth ability and colony formation ability of cancer cells ( 17 - 19 ). Unlike other MMP members, MMP11 has unique functions and signaling pathways.…”