Aim: To investigate the role and function of NOL6, a protein related to ribosome biogenesis, in endometrial cancer. Methods: Methyl thiazolyl tetrazolium assay, colony formation assay, flow cytometry apoptosis assay, transwell assay and wound healing assays were carried out for evaluating cell proliferation, migration and apoptosis. Immunohistochemistry, western blot and tumor xenograft assays were carried out for detecting the level of protein expression and tumor formation. Results: We demonstrated that NOL6 is overexpressed in endometrial cancer and promotes cell proliferation and migration while reducing apoptosis. NOL6 regulates the expression of TWIST1, which can restore the changes in cells caused by NOL6 knockdown. Conclusions: NOL6 can promote the proliferation and migration of endometrial cancer cells by regulating TWIST1 expression.
Keywords: NOL6; TWIST1; epithelial–mesenchymal transition; nucleolar protein; tumorigenesis.
Lay abstract In endometrial cancer, rapid tumor growth leads to increased protein synthesis and ribosome biogenesis. Our study confirmed the involvement of the protein NOL6 in endometrial cancer. We overexpressed TWIST1, MMP2 or MYC in endometrial cells and assessed the difference in cell growth, spread, death and tumor formation under different conditions. The results showed that NOL6 can boost the growth and spread of endometrial cancer cells by controlling TWIST1 expression. Our study provides a new understanding of the molecular mechanisms causing endometrial cancer.