| Literature DB >> 35094303 |
Abstract
NPC is a type of cancer with a poor prognosis. We aim to excavate the regulatory roles of miR-135b-5p in NPC and uncover the underlying mechanism. The levels of miR-135b-5p and Sirtuin 1 (SIRT1) in NPC and normal tissues and cells were tested via quantitative real-time PCR, western blotting, and immunohistochemistry, respectively. The binding relationship between them was predicted with ENCORI databases and validated with dual-luciferase reporter assay. The impact of miR-135b-5p and SIRT1 on the expressions of matrix metalloproteinase 7 (MMP7) and epithelial-mesenchymal transformation (EMT) proteins in NPC cells was evaluated by western blotting. Metastasis of NPC cells was evaluated by Transwell assay. The binding of c-JUN at the MMP7 promoter and deacetylation of c-JUN were examined using chromatin-immunoprecipitation and co-immunoprecipitation, respectively. The level of miR-135b-5p was increased and SIRT1 was decreased in NPC tissues and cells. miR-135b-5p was validated to target SIRT1. Silencing of miR-135b-5p accelerated EMT and metastasis of NPC cells, whereas knockdown of SIRT1 showed opposite results. Notably, knockdown of SIRT1 partially reversed the miR-135b-5p-induced change of EMT markers and metastasis of NPC cells. Mechanistically, miR-135b-5p disrupted SIRT1-induced deacetylation of c-JUN to promote the activation of MMP7 in NPC cells. miR-135b-5p targeted SIRT1 to inhibit deacetylation of c-JUN and increase MMP7 expression to promote malignancy of NPC cells.Entities:
Keywords: Invasion; MMP7; Migration; Nasopharyngeal carcinoma; SIRT1; c-JUN; miR-135b-5p
Mesh:
Substances:
Year: 2022 PMID: 35094303 DOI: 10.1007/s12033-022-00457-5
Source DB: PubMed Journal: Mol Biotechnol ISSN: 1073-6085 Impact factor: 2.695