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Human endogenous retroviral K element encodes fusogenic activity in melanoma cells.

Huang G, Li Z, Wan X, Wang Y, Dong J.

J Carcinog. 2013 Mar 16;12:5.

Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, USA ; Sealy Center for Cancer Biology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, USA.

 

Abstract

 

INTRODUCTION AND HYPOTHESIS:

Nuclear atypia with features of multi nuclei have been detected in human melanoma specimens. We found that the K type human endogenous retroviral element (HERV K) is expressed in such cells. Since cellular syncytia can form when cells are infected with retroviruses, we hypothesized that HERV K expressed in melanoma cells may contribute to the formation of multinuclear atypia cells in melanoma.

EXPERIMENTS AND RESULTS:

We specifically inhibited HERV K expression using RNA interference (RNAi) and monoclonal antibodies and observed dramatic reduction of intercellular fusion of cultured melanoma cells. Importantly, we identified loss of heterozygosity (LOH)of D19S433 in a cell clone that survived and proliferated after cell fusion.

CONCLUSION:

Our results support the notion that proteins encoded by HERV K can mediate intercellular fusion of melanoma cells, which may generate multinuclear cells and drive the evolution of genetic changes that provide growth and survival advantages.

KEYWORDS:

Cell fusion, K-type human endogenous retroviral deoxyribonucleic acid, melanoma

 

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Additional Information

Nuclear atypia with features of multinuclei have been detected in human melanoma specimens. The study found that the K-type human endogenous retroviral element (HERV-K) is expressed in such cells. Since cellular syncytia can form when cells are infected with retroviruses, the studyhypothesized that HERV-K, which is expressed in melanoma cells and may play a role in melanomagenesis, contributes to the formation of multinuclear cells in melanoma. The study specifically inhibited HERV-K using RNAi and monoclonal antibodies and observed dramatic reduction of colony formation and intercellular fusion of cultured melanoma cells. The study also identified loss of heterozygosity (LOH) of D19S433 in a cell clone that survived and proliferated after cell fusion. The same research group has reported previously that the activation of HERV-K is regulated by MEK and CDK4 pathways. The present study further the analysis of HERV-K in melanoma and supports the notion that activated HERV-K can mediate intercellular fusion of melanoma cells, which may cause molecular changes in tumor cells that can provide growth and survival advantages.

 

Human endogenous retroviral K element encodes fusogenic activity in melanoma cells