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SIRT7 suppresses the epithelial-to-mesenchymal transition in oral squamous cell
carcinoma metastasis by promoting SMAD4 deacetylation
#MMPMID30001742
Li W
; Zhu D
; Qin S
J Exp Clin Cancer Res
2018[Jul]; 37
(1
): 148
PMID30001742
show ga
BACKGROUND: Oral squamous cell carcinoma (OSCC) is one of the most common
malignancies and has a poor prognosis. The epithelial-to-mesenchymal transition
(EMT) is crucial for increasing the metastasis of OSCC. Recently, studies have
indicated that sirtuin7 (SIRT7) is implicated in tumor genesis; however, the
potential role of SIRT7 in the EMT and metastasis of OSCC has not been reported.
METHODS: We investigated the cellular responses to SIRT7 silencing or
overexpression in OSCC cell lines by wound healing assay, migration and invasion
assay, western blotting, immunofluorescence and immunohistochemistry. RESULTS: In
the present study, we found that SIRT7 was significantly downregulated in OSCC
cell lines and human OSCC/OSCC tissues with lymph node metastasis. Overexpression
of SIRT7 decreased the proliferation and invasion of OSCC cells in vitro, whereas
SIRT7 knockdown significantly increased OSCC cell growth and invasion.
Upregulation of SIRT7 concomitantly increased the expression of E-cadherin, and
decreased the expression of mesenchymal markers. SIRT7 overexpression also
reduced the level of acetylated SMAD4 in OSCC cells. Moreover, SIRT7
overexpression significantly inhibited OSCC lung metastasis in vivo. CONCLUSION:
Together, these findings suggested that SIRT7 suppressed EMT in OSCC metastasis
by promoting SMAD4 deacetylation.
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