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Sirtuin 7 promotes colorectal carcinoma proliferation and invasion through the inhibition of E-cadherin

Sirtuin 7 (Sirt7) is a member of the sirtuin protein family and is implicated in various carcinomas; however, the function of Sirt7 in colorectal carcinoma (CRC) remains unclear. The present study aimed to explore the biological function of Sirt7 in CRC tissues and cell lines, and to investigate the...

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Detalles Bibliográficos
Autores principales: Deng, Zhigang, Wang, Xingbiao, Long, Xuan, Liu, Wanzhong, Xiang, Chunhua, Bao, Feng, Wang, Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5792759/
https://www.ncbi.nlm.nih.gov/pubmed/29467843
http://dx.doi.org/10.3892/etm.2017.5673
Descripción
Sumario:Sirtuin 7 (Sirt7) is a member of the sirtuin protein family and is implicated in various carcinomas; however, the function of Sirt7 in colorectal carcinoma (CRC) remains unclear. The present study aimed to explore the biological function of Sirt7 in CRC tissues and cell lines, and to investigate the potential underlying mechanism by performing reverse transcription-quantitative polymerase chain reaction analyses, western blot analyses, luciferase reporter assays, cell proliferation and invasion assays. It was demonstrated that Sirt7 presented a higher expression in CRC tissues and cell lines compared with that in normal tissues and cells, and this higher expression was correlated with the tumor size, the tumor, node and metastasis stage and distant metastasis. Knockdown of Sirt7 repressed the proliferation ability of SW620 and HCT116 cells in vitro, while ectopic expression of Sirt7 increased the epithelial-mesenchymal transition and invasion in HT29 and SW480 cells. Notably, these functional effects of Sirt7 were exerted through the repression of E-cadherin. Thus, the data of the present study indicated a novel mechanistic role for Sirt7 as an oncogene in CRC malignancy, and Sirt7 may be a potential therapeutic target.