In this study, we found that SIRT7 expression was elevated in papillary thyroid cancers (PTCs), and demonstrated that SIRT7 knockdown dramatically inhibited the proliferation, colony formation, migration and invasion of thyroid cancer cells, and induced thyroid cancer cell cycle arrest and apoptosis.
The findings of the present study indicated that Sirt7 affects the malignancy of glioma cells mainly in promoting glioma proliferation and invasion through ERK and STAT3 signaling.
Knockdown of Sirt7 repressed the proliferation ability of SW620 and HCT116 cells <i>in vitro</i>, while ectopic expression of Sirt7 increased the epithelial-mesenchymal transition and invasion in HT29 and SW480 cells.
Overexpression of SIRT7 decreased the proliferation and invasion of OSCC cells in vitro, whereas SIRT7 knockdown significantly increased OSCC cell growth and invasion.
Notably, the overexpression of SIRT7 promoted the proliferation and invasion of angiosarcoma cells and also partially reversed the antitumor effect of miR-340 on angiosarcoma cell proliferation and invasion.
We also demonstrated that the knock down of SIRT7 decreased the migration of DU145 and PC3 cells (two androgen-independent prostate cancer cell lines) whereas the overexpression of the native protein but not the mutated form increased the cell migration and the invasion of the poorly aggressive prostate cancer cell line LNCaP.
Furthermore, the silencing of CDC4 partially rescued SIRT7 knockdown-mediated inhibitory effects on proliferation, migration, and invasion of osteosarcoma cells.
In Sirt7-overexpressing cells, the mesenchymal markers vimentin and fibronectin were upregulated, and the epithelial markers E-cadherin and β-catenin were downregulated, which was linked to enhanced invasion by colorectal cancer cells.