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Analysis of HERV-K (HML2) Expression in Colorectal Cancer Samples.

Valentina S Obrezanenko1, Polina M Shulga1, Anastasia G Volkova1

  • 1Federal State Budgetary Institution «Centre for Strategic Planning and Management of Biomedical Health Risks», Federal Medical and Biological Agency (Centre for Strategic Planning, of the Federal Medical and Biological Agency), Moscow 123182, Russia.

Epigenomes
|February 20, 2026
PubMed
Summary

Human endogenous retrovirus K (HERV-K) elements are expressed differently in colorectal cancer (CRC) molecular subtypes. Their expression inversely correlates with DNA methylation, suggesting a role in CRC pathogenesis.

Keywords:
CMSDNA methylationHERV-K (HML-2)RNA-seqcolorectal cancerviral mimicry

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Area of Science:

  • Genomics
  • Epigenetics
  • Cancer Biology

Background:

  • Human endogenous retrovirus K (HERV-K) elements, specifically the HML-2 subgroup, are implicated in cancer development.
  • However, their expression and epigenetic regulation across colorectal cancer (CRC) molecular subtypes are not fully understood.

Purpose of the Study:

  • To investigate HML-2 expression patterns in different colorectal cancer (CRC) molecular subtypes.
  • To explore the epigenetic regulation, specifically DNA methylation, of HML-2 elements in CRC.

Main Methods:

  • RNA-sequencing and DNA methylation data from paired CRC and normal tissues were analyzed.
  • HERV-K expression was quantified using bioinformatics tools (Telescope, TEtranscripts, GeneTEFlow) and validated with RT-PCR.
  • Colorectal cancer molecular subtypes (CMSs) were determined using CMScaller.

Main Results:

  • Consistent HML-2 expression levels were observed across multiple bioinformatics tools.
  • Differential HML-2 expression was identified across various CMS subtypes of CRC.
  • An inverse correlation between HML-2 locus expression and CpG site methylation was found in all CMSs.
  • HML-2 expression was associated with specific genes (e.g., CR1, CD48) involved in CRC pathogenesis.
  • Expression signatures linked to RIG-I-like receptor signaling were detected in CMS1-3, suggesting viral mimicry.

Conclusions:

  • HML-2 expression and its epigenetic regulation via DNA methylation are integral to understanding colorectal cancer (CRC) pathogenesis.
  • These findings highlight the complex interplay between endogenous retroelements and cancer development across molecular subtypes.