Knockdown of Linc00511 inhibits TGF-β-induced cell migration and invasion by suppressing epithelial-mesenchymal transition and down-regulating MMPs expression.

Biomed Pharmacother

Department of Cardiothoracic Surgery, Xinhua Hospital, School of medicine, Shanghai Jiao Tong University, Shanghai 200092, PR China. Electronic address:

Published: May 2020

Epithelial mesenchymal transition (EMT) is a critical step in cancer metastasis. Some evidences have been provided to verify up-regulation of linc00511 in multiple cancers and oncogenic roles during cancer malignant process. But, the roles of linc00511 on the metastasis of lung cancer are still largely unclear. Our study aims to reveal the functional effects of linc00511 on TGF-β1-induced EMT in lung cancer. Our results showed that knockdown of linc00511 significantly inhibited TGF-β1-induced migration and invasion and down-regulated the mRNA and protein levels of MMP2, MMP9 and MMP12 in TGF-β1 treated SPCA1 and H1975 cells. Also, western blotting results showed that inhibition of linc00511 remarkably suppressed TGF-β1-induced N-cadherin, Vimentin and snail and increased E-cadherin expression in SPCA1 and H1975 cells. Noteworthy, we further found that inhibition of linc00511 could down-regulate TGF-β1-induced ZEB2 mRNA and protein levels by sponging miR-183-5p in SPCA1 and H1975 cells. Taken together, our findings suggested knockdown linc00511 suppressed TGF-β1-induced migration and invasion via inhibiting EMT and MMPs in lung cancer cells.

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http://dx.doi.org/10.1016/j.biopha.2019.109049DOI Listing

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