Viruses in colorectal cancer

Area of Science:

• Oncology
• Virology
• Microbiome Research

Background:

• Colorectal cancer (CRC) development is influenced by microbial cofactors, but mechanisms involving viruses remain poorly understood.
• While Epstein-Barr virus (EBV), human papillomavirus (HPV), and John Cunningham virus (JCV) are known carcinogens in CRC, cytomegalovirus (CMV) also shows associations.
• Emerging research highlights bacteriophages as potential modulators in CRC carcinogenesis and progression.

Purpose of the Study:

• To review how viruses and bacteriophages impact cellular and microenvironmental interactions in colorectal cancer.
• To explore the potential mechanisms by which these microorganisms contribute to CRC oncogenesis and progression.
• To discuss the common oncogenic pathways affected by viruses such as EBV, CMV, HPV, and JCV in CRC.

Main Methods:

• Literature review summarizing current evidence on viral and bacteriophage involvement in CRC.
• Analysis of proposed mechanisms including DNA damage, chromosomal instability, and cell proliferation.
• Examination of viral impacts on key signaling pathways like Wnt/β-catenin, p53, pRb, EMT, and EGFR.

Main Results:

• Viruses can promote CRC by inducing DNA damage, chromosomal instability, and altering cell proliferation and metastasis.
• Common viral oncogenic features include latent infections and modulation of p53, pRb, EMT, EGFR, and Wnt/β-catenin pathways.
• The complex interplay within the gut microbiome, including phages, bacteria, and viruses, complicates establishing direct causal links between specific infections and CRC.

Conclusions:

• Viruses and bacteriophages are significant potential cofactors in colorectal cancer development and progression.
• Understanding viral-host and viral-microbial interactions is crucial for elucidating CRC pathogenesis.
• Further research is needed to unravel the complex roles of the microbiome and specific pathogens in CRC etiology.