Back to Journals » OncoTargets and Therapy » Volume 11

E2F3 promotes cancer growth and is overexpressed through copy number variation in human melanoma

Authors Feng Z, Peng C, Li D, Zhang D, Li X, Cui F, Chen Y, He Q

Received 14 May 2018

Accepted for publication 5 July 2018

Published 30 August 2018 Volume 2018:11 Pages 5303—5313

DOI https://doi.org/10.2147/OTT.S174103

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Takuya Aoki


Video abstract of "E2F3 promotes cancer growth and is overexpressed through copy number variation in human melanoma" [ID 174103]

Views: 37

Zhicai Feng,1 Cheng Peng,1 Daojiang Li,2 Danhua Zhang,3 Xu Li,1 Fengran Cui,1 Yanhong Chen,4 Quanyong He1

1Department of Burns and Plastic Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China; 2Department of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China; 3Department of Medical Laboratory, Huakang Hospital, Dazhou, Sichuan, China; 4Fujian Medical University, Fuzhou, Fujian, China

Introduction: Melanoma is a malignant tumor that seriously affects patients. The pathogenesis of malignant melanoma is complex, and the cell cycle is closely related to tumor progression. Based on the catalog of cancer somatic mutations, we found that overexpression of the E2F3 gene ranked first in percentage increase in not only melanoma but also in all human cancer tissues. However, there are few studies on the high expression of E2F3 and its carcinogenic mechanism in melanoma.
Methods and results: We found that E2F3 showed extensive copy number amplification that was positively correlated with the expression level. Patients with high copy number had a significantly poorer prognosis. We also found that E2F3 levels were significantly negatively correlated with promoter methylation. However, we showed that the E2F3 promoter region is hypomethylated, and in normal cells or tumor cells, the methylation level did not correlate with expression. Finally, we knocked down the E2F3 gene in melanoma cells by shRNA. Colony formation, anchorage-dependent growth, and EdU cell proliferation experiments showed a significant decrease in proliferation. Flow cytometry showed a significant increase in the G0/G1 ratio.
Conclusion: It can be speculated that copy number amplification and other mechanisms result in the high expression of E2F3 in melanoma, which promotes tumor progression by involving the cell cycle. E2F3 is a good target for the treatment of melanoma.

Keywords: E2F3, melanoma, mechanism, overexpression, copy number, methylation

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]