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Updated: Aug 1, 2025

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
Published on: January 7, 2019
Anti-HERV-K Drugs and Vaccines, Possible Therapies against Tumors
Sepideh Hosseiniporgham1, Leonardo Antonio Sechi1,2
1Department of Biomedical Sciences, University of Sassari, 07100 Sassari, Italy.
Abstract:
The footprint of human endogenous retroviruses (HERV), specifically HERV-K, has been found in malignancies, such as melanoma, teratocarcinoma, osteosarcoma, breast cancer, lymphoma, and ovary and prostate cancers. HERV-K is characterized as the most biologically active HERV due to possession of open reading frames (ORF) for all Gag, Pol, and Env genes, which enables it to be more infective and obstructive towards specific cell lines and other exogenous viruses, respectively. Some factors might contribute to carcinogenicity and at least one of them has been recognized in various tumors, including overexpression/methylation of long interspersed nuclear element 1 (LINE-1), HERV-K Gag, and Env genes themselves plus their transcripts and protein products, and HERV-K reverse transcriptase (RT). Therapies effective for HERV-K-associated tumors mostly target invasive autoimmune responses or growth of tumors through suppression of HERV-K Gag or Env protein and RT. To design new therapeutic options, more studies are needed to better understand whether HERV-K and its products (Gag/Env transcripts and HERV-K proteins/RT) are the initiators of tumor formation or just the disorder's developers. Accordingly, this review aims to present evidence that highlights the association between HERV-K and tumorigenicity and introduces some of the available or potential therapies against HERV-K-induced tumors.
Insights
Human endogenous retroviruses (HERV), particularly HERV-K, are linked to various cancers. This review explores HERV-K
Area of Science:
- Oncology
- Virology
- Genetics
Background:
- Human endogenous retroviruses (HERV), especially HERV-K, are implicated in numerous cancers, including melanoma and breast cancer.
- HERV-K's biological activity stems from complete open reading frames (ORF) for Gag, Pol, and Env genes, enhancing infectivity and viral obstruction.
- Tumorigenesis may involve HERV-K products like Gag, Env, and reverse transcriptase (RT), alongside LINE-1 elements, through overexpression or methylation.
Purpose of the Study:
- To review the association between HERV-K and tumorigenicity.
- To present evidence linking HERV-K to cancer development.
- To introduce current and potential therapies for HERV-K-associated tumors.
Main Methods:
- Literature review of studies on HERV-K and cancer.
- Analysis of evidence linking HERV-K gene products to tumor formation.
- Compilation of information on therapeutic strategies targeting HERV-K.
Main Results:
- HERV-K's presence and activity are documented across diverse malignancies.
- Overexpression/methylation of HERV-K components (Gag, Env, RT) and LINE-1 are observed in tumors.
- Current therapies focus on suppressing HERV-K products or managing autoimmune responses.
Conclusions:
- HERV-K plays a significant role in tumorigenesis, though its exact role as an initiator or promoter requires further investigation.
- Understanding HERV-K's involvement is crucial for developing targeted therapies.
- Further research is needed to elucidate the precise mechanisms of HERV-K in cancer and refine therapeutic approaches.
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