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Published on: May 11, 2016
The Role of HERV-K in Cancer Stemness
Sarah R Rivas1, Mynor J Mendez Valdez2, Vaidya Govindarajan2
1Surgical Neurology Branch, National Institute of Neurological Diseases and Stroke, Bethesda, MD 20892, USA.
Abstract:
Human endogenous retrovirus-K (HERV-K) is the most recently integrated retrovirus in the human genome, with implications for multiple disorders, including cancer. Although typically transcriptionally silenced in normal adult cells, dysregulation of HERV-K (HML-2) elements has been observed in cancer, including breast, germ cell tumors, pancreatic, melanoma, and brain cancer. While multiple methods of carcinogenesis have been proposed, here we discuss the role of HERV-K (HML-2) in the promotion and maintenance of the stem-cell in cancer. Aberrant expression of HERV-K has been shown to promote expression of stem cell markers and promote dedifferentiation. In this review, we discuss HERV-K (HML-2) as a potential therapeutic target based on evidence that some tumors depend on the expression of its proteins for survival.
Insights
Human endogenous retrovirus-K (HERV-K) is implicated in cancer by promoting stemness. Targeting HERV-K (HML-2) proteins may offer a novel therapeutic strategy for various cancers.
Area of Science:
- Oncology
- Virology
- Genetics
Background:
- Human endogenous retrovirus-K (HERV-K) is the most recent retroviral addition to the human genome.
- HERV-K (HML-2) elements are usually silenced in healthy adults but are dysregulated in various cancers.
- Aberrant HERV-K expression is linked to cancer stem cell characteristics and dedifferentiation.
Purpose of the Study:
- To review the role of HERV-K (HML-2) in cancer promotion and maintenance.
- To explore HERV-K (HML-2) as a potential therapeutic target in oncology.
Main Methods:
- Literature review of studies investigating HERV-K (HML-2) expression in cancer.
- Analysis of evidence linking HERV-K (HML-2) to cancer stem cell properties.
- Evaluation of HERV-K (HML-2) protein dependency in tumor survival.
Main Results:
- Dysregulated HERV-K (HML-2) elements are observed across multiple cancer types, including breast, germ cell, pancreatic, melanoma, and brain cancers.
- HERV-K (HML-2) expression promotes stem cell markers and dedifferentiation, contributing to cancer stemness.
- Certain tumors exhibit dependency on HERV-K (HML-2) proteins for their survival.
Conclusions:
- HERV-K (HML-2) plays a significant role in the promotion and maintenance of cancer stem cells.
- HERV-K (HML-2) represents a promising therapeutic target for cancer treatment.
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