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Decoding microbial carcinogenic strategies: ubiquitination and SUMO modification.

Yue Liu1,2, Xianghai Zeng1,2, Zhimai Lyu2

  • 1School of Basic Medicine, Gannan Medical University, Ganzhou, Jiangxi, China.

Frontiers in Microbiology
|January 5, 2026
PubMed
Summary

Carcinogenic microorganisms, especially viruses, hijack the host ubiquitin-proteasome system (UPS) and SUMOylation networks to cause cancer. Targeting these pathways offers new precision cancer therapy strategies.

Keywords:
carcinogenic microorganismsinfection-associated carcinogenesistargeted therapiestumorigenesis mechanismsubiquitin-SUMO axis

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Area of Science:

  • Molecular Biology
  • Oncology
  • Microbiology

Background:

  • Carcinogenic microorganisms disrupt cellular homeostasis to promote tumorigenesis.
  • Oncogenic viruses, bacteria, and fungi exploit host regulatory networks.
  • The ubiquitin-proteasome system (UPS) and SUMOylation are key cellular processes implicated in cancer.

Purpose of the Study:

  • To elucidate the mechanisms by which carcinogenic microorganisms manipulate the UPS and SUMOylation networks.
  • To highlight the role of oncogenic viruses in hijacking these host systems for tumor promotion.
  • To identify potential molecular targets for precision cancer therapy.

Main Methods:

  • Review of existing literature on microbial carcinogenesis and host UPS/SUMOylation pathways.
  • Analysis of specific viral proteins (e.g., HPV E6, HBV HBx, HCV core, EBV LMP1, KSHV K3) and their interactions with UPS/SUMOylation components.
  • Examination of non-viral microbial factors (e.g., H. pylori CagA, aflatoxin A) involved in UPS/SUMOylation regulation.

Main Results:

  • Oncogenic viruses utilize diverse strategies to modulate UPS/SUMOylation, including protein degradation, epigenetic alterations, and immune evasion.
  • HPV E6 targets p53 degradation; HBV HBx inhibits E3 ligase SIAH1; HCV core blocks its degradation; EBV LMP1 activates NF-xB; KSHV K3 mediates immune evasion.
  • Non-viral agents like H. pylori CagA and aflatoxin A also regulate these critical cellular pathways.

Conclusions:

  • Targeted modulation of the UPS/SUMO system is a central oncogenic strategy employed by carcinogenic microorganisms.
  • Understanding these microbial hijacking mechanisms provides crucial insights for developing novel precision cancer therapies.
  • The UPS/SUMOylation network represents a promising therapeutic target for cancers associated with microbial infections.