NOL6 Promotes the Proliferation and Migration of Endometrial Cancer Cells by Regulating TWIST1 Expression

Abstract

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.

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.

Keywords::

• epithelial–mesenchymal transition
• NOL6
• nucleolar protein
• tumorigenesis
• TWIST1

Author contributions

Study concept and design: H Zhang and Changzhong Li. Acquisition of data: J Liang, W Sun and Q Li. Analysis and interpretation of data: J Liang, H Song and Y Zhao. Drafting of the manuscript: J Liang. Critical revision of the manuscript for important intellectual content: H Zhang, Chunyan Li and C Wang. Statistical analysis: J Liang and H Zhang. Obtained funding: H Zhang, D Wei and Changzhong Li. Study supervision: H Zhang and Changzhong Li. All authors have contributed significantly and are in agreement with the content of the manuscript.

Financial & competing interests disclosure

The research was supported by grants from Science and Technology Development Program of Jinan (no. 201805023), Shandong Province medical and health technology development projects (no. 2016WS0442, 2016WS0404, 2017WS191), National Natural Science Foundation of China (no. 81300468; no. 81671433; no. 81671434) and Natural Science Foundation of Shandong Province (ZR2016HQ22). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Ethical conduct of research

All authors state that we have obtained Institutional Ethics Committee approval for all human (no. 2016-KY-015) or animal (no. 2020-904) experimental investigations. In addition, for investigations involving human subjects, informed consent has been obtained from the participants involved.

Additional information

Funding

The research was supported by grants from Science and Technology Development Program of Jinan (no. 201805023), Shandong Province medical and health technology development projects (no. 2016WS0442, 2016WS0404, 2017WS191), National Natural Science Foundation of China (no. 81300468; no. 81671433; no. 81671434) and Natural Science Foundation of Shandong Province (ZR2016HQ22). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.