J Cancer 2019; 10(20):4954-4960. doi:10.7150/jca.31544 This issue

Research Paper

The voltage-gated sodium channel Nav1.7 associated with endometrial cancer

Junxiu Liu1*, Hao Tan1*, Wancai Yang2, Shuzhong Yao1✉, Liang Hong2✉

1. Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
2. Institute of Precision Medicine, Jining Medical University, Jining, China.
*These authors contributed equally to this work.

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Liu J, Tan H, Yang W, Yao S, Hong L. The voltage-gated sodium channel Nav1.7 associated with endometrial cancer. J Cancer 2019; 10(20):4954-4960. doi:10.7150/jca.31544. Available from https://www.jcancer.org/v10p4954.htm

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Background: Endometrial cancer is the most common gynecologic malignancy in women in the developed countries. Despite recent progress in functional characterization of voltage-gated sodium channel (Nav) in multiple cancers, very little was known about the expression of Nav in human endometrial cancer. The present study sought to determine the role of Nav and molecular nature of this channel in the endometrial cancer.

Methods: PCR approach was introduced to determine expression level of Nav subunits in endometrial cancer specimens. Pharmacological agents were used to investigate Nav function in endometrial cancer cells. Flow cytometry were used to test cancer apoptosis, and invasion assays were applied to test tumor metastasis.

Results: Transcriptional levels of the all Nav α and β subunits were determined by real time-PCR in endometrial cancer with pair tissues of carcinoma and adjacent nonneoplastic tissue, Nav1.7 was the most highly expressed Nav subtype in endometrial cancer tissues. Nav1.7 level was closely associated with tumor size, local lymph node metastasis, and 5-year and 10-year survival ratio. Inhibition of this channel by Nav1.7 blocker PF-05089771, promoted cancer apoptosis and attenuated cancer cell invasion.

Conclusion: These results establish a relationship between voltage-gated sodium channel protein and endometrial cancer, and suggest that Nav1.7 is a potential prognostic biomarker and could serve as a novel therapeutic target for endometrial cancer.

Keywords: Endometrial Cancer, Nav1.7, Voltage-Gated Sodium Channel, Ion Channels.