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Correspondence
Elevation of human ERV3-1 env protein expression in colorectal cancer
  1. Seung-Hyun Lee1,
  2. Yun-Jeong Kang2,
  3. Jin-Ok Jo2,
  4. Mee Sun Ock2,
  5. Kyung-Wan Baek3,
  6. Jungwoo Eo4,
  7. Woo Jae Lee4,
  8. Yung Hyun Choi5,
  9. Wun-Jae Kim6,
  10. Sun-Hee Leem7,
  11. Heui-Soo Kim4,
  12. Hee-Jae Cha1,8
  1. 1 Department of Surgery, Kosin University College of Medicine, Busan, Republic of Korea
  2. 2 Department of Parasitology and Genetics, Kosin University College of Medicine, Busan, Republic of Korea
  3. 3 Division of Sports Science, Department of Sports Science, Pusan National University, Busan, Republic of Korea
  4. 4 Department of Biological Sciences, College of Natural Sciences, Pusan National University, Busan, Republic of Korea
  5. 5 Department of Biochemistry, College of Oriental Medicine, Dongeui University, Busan, Republic of Korea
  6. 6 Department of Urology, Chungbuk National University College of Medicine, Cheongju, Republic of Korea
  7. 7 Department of Biological Science, Dong-A University, Busan, Republic of Korea
  8. 8 Institute for Medical Science, Kosin University College of Medicine, Busan, Republic of Korea
  1. Correspondence to Professor Hee-Jae Cha, Departments of Parasitology and Genetics, Kosin University College of Medicine, Busan 602-702, Republic of Korea; hcha{at}kosin.ac.kr Professor Heui-Soo Kim, Department of Biological Sciences, College of Natural Sciences, Pusan National University, Busan 609-735, Republic of Korea; khs307{at}pusan.ac.kr.

https://doi.org/10.1136/jclinpath-2013-202089

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    The endogenous retrovirus (ERV) appeared in the vertebrate genome millions of years ago, but is now inactivated due to mutations such as deletions or nonsense mutations. After the mutation, ERV eventually became fixed in the genome in its endogenous form. In the case of human ERV (HERV), 98 000 ERV elements or fragments were inserted into the human genome, which is approximately 8% of the whole genome.1 HERV is defective and unable to replicate and only traces of the original viruses exist in the human genome.2 Even though HERVs have been reported to be inactive, there are several studies showing the relationship between HERVs and some diseases including cancers. Contreras-Galindo et al3 first showed that HERV-K genes are significantly upregulated in the plasma of lymphoma and breast cancer patients and that there are virus-like particles in the plasma of lymphoma patients. Many other studies have shown that HERV-K can be a good model for immunotherapeutic targets4 and is a biomarker of early-stage breast cancer.5 Additionally, there have been reports demonstrating that HERV-K is involved in breast cancer,4–⇓6 prostate cancer,7 melanoma8 and ovarian cancer.9 ERV3-1 (HERV-R) is related to lymphoma10 and HERV-E is upregulated in urothelial carcinoma11 and colon cancer.12

    We recently reported that the ERV3-1 (HERV-R) env protein is expressed in both adult human organs and tumours using a tissue microarray. We also compared the expression of ERV3-1 between normal and tumour tissues to study the relationship between ERV3-1 and tumour formation. ERV3-1 was highly expressed in certain types of tumours, including lung adenocarcinoma, renal cell carcinoma, papillary carcinoma, hepatocellular carcinoma and adenocarcinoma in the gastrointestinal tract.13 Although …

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    Footnotes

    • Contributors H-JC, S-HL and H-SK: designed the research and wrote the manuscript; Y-JK, J-OJ, MSO, K-WB, JE and WJL: performed the experiments and analysed data; YHC, W-JK and S-HL: supervised drafting of the final manuscript.

    • Funding This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Korean government (2008-0062611).

    • Competing interests None.

    • Patient consent Obtained.

    • Ethics approval National Biobank of Korea institutional review board.

    • Provenance and peer review Not commissioned; externally peer reviewed.