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.

中文翻译：

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linc00511 敲低通过调节 miR-16-5p/MMP11 抑制肺癌进展

肺癌（LC）是一种对人类危害极大的恶性肿瘤。根据大量研究，长链非编码 RNA (lncRNA) 与 LC 的发展密不可分。这项工作旨在鉴定 LC 中 linc00511 的表达，并挖掘 linc00511 调节 LC 进展的潜在机制。实验结果显示，linc00511在LC中明显上调，并且linc00511敲低显着损害LC细胞的体外恶性表型。为了深入研究linc00511对LC进展的贡献，发现miR-16-5p具有与linc00511序列的结合位点，这也反向影响linc00511在LC中的表达。进一步的实验数据表明，miR-16-5p 直接且负向靶向基质金属肽酶 11 (MMP11)。此外，救援实验表明，miR-16-5p 抑制或 MMP11 过表达抵消了 linc00511 沉默对 LC 进展的抑制影响。综上所述，我们的研究结果表明，linc00511 在促进 LC 进展中发挥着至关重要的作用，机制研究表明 linc00511 通过靶向 miR-16-5p/MMP11 轴加剧了 LC 进展。