Expression of HERV-K Correlates With Status of MEK–ERK and p16INK4A–CDK4 Pathways in Melanoma Cells

Zhongwu LiSealy Center for Cancer Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA, Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA

Tao ShengSealy Center for Cancer Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA, Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA

Xiaohua WanSealy Center for Cancer Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA, Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA

Tianshuang LiuSealy Center for Cancer Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA, Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA

Hai WuSealy Center for Cancer Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA, Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA

Jianli DongSealy Center for Cancer Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA, Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA

ABSTRACT

The dysregulated ERK and RB pathways often coexist in melanoma cells. The K-type human endogenous retrovirus (HERV-K) is implicated in melanomagenesis. Some of the phenotypes that are modified by HERV-K (e.g., changes in cell shape, melanin production, and anchorage-dependent growth) overlap with those that are regulated by ERK and RB pathways. As ERK signaling can regulate retroviruses, we hypothesized that HERV-K expression is controlled by ERK–RB pathways. We found that the levels of HERV-K GAG and EVE correlated with the activation of ERK and loss of p16INK4A and that inhibition of MEK or CDK4, especially in combination, reduced HERV-K EVE in melanoma cells.

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Expression of HERV-K Correlates With Status of MEK–ERK and p16INK4A–CDK4 Pathways in Melanoma Cells

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Expression of HERV-K Correlates With Status of MEK–ERK and p16INK4A–CDK4 Pathways in Melanoma Cells

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