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Enteroviral epitope mimicry enables NK cell-mediated targeting of ASPH in hepatocellular carcinoma
Man Hsin Hung1, Qin Li1, Limin Wang1
1Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892.
Abstract:
Cancer development is shaped by host-microbe interactions, including viral infections. While several viruses are established oncogenic drivers, their potential protective roles in cancer remain unclear. Here we identify a dominant antibody response to CE1, a consensus epitope of enterovirus and rhinovirus, that is associated with reduced hepatocellular carcinoma (HCC) incidence and mortality. Anti-CE1 antibodies selectively recognize HCC cells and mediate anti-tumor activity through NK cell-mediated antibody-dependent cellular cytotoxicity (ADCC). Mechanistically, anti-CE1 antibodies cross-react with aspartate β-hydroxylase (ASPH), with CE1-ASPH sequence homology underpinning tumor recognition and cytotoxicity. Clinically, ASPH is aberrantly upregulated in HCC and correlates with inferred NK cell-associated ADCC activity and improved survival in CE1-seropositive patients. Collectively, these findings reveal a mechanism by which antiviral humoral immunity confers cancer protection through molecular mimicry and highlight anti-CE1 immunity as a potential therapeutic strategy in HCC.
Insights
Antiviral immunity may protect against cancer. Antibodies targeting enterovirus (CE1) recognize and kill liver cancer cells by mimicking a tumor protein, suggesting a new cancer therapy.
Area of Science:
- Immunology
- Oncology
- Virology
Background:
- Host-microbe interactions, including viral infections, influence cancer development.
- While oncogenic viruses are known, protective roles of viral infections in cancer are unclear.
Purpose of the Study:
- To investigate the protective role of antiviral immunity in cancer.
- To identify mechanisms of anti-tumor activity mediated by antiviral antibodies.
Main Methods:
- Identified antibody responses to a consensus enterovirus/rhinovirus epitope (CE1).
- Assessed anti-CE1 antibody recognition of hepatocellular carcinoma (HCC) cells.
- Investigated NK cell-mediated antibody-dependent cellular cytotoxicity (ADCC).
- Analyzed cross-reactivity between anti-CE1 antibodies and tumor-associated antigens, specifically aspartate β-hydroxylase (ASPH).
Main Results:
- A dominant anti-CE1 antibody response was associated with reduced HCC incidence and mortality.
- Anti-CE1 antibodies recognized HCC cells and mediated anti-tumor ADCC.
- Antibodies cross-reacted with ASPH due to sequence homology, enabling tumor recognition.
- ASPH upregulation in HCC correlated with improved survival in CE1-seropositive patients.
Conclusions:
- Antiviral humoral immunity can confer cancer protection via molecular mimicry.
- Anti-CE1 immunity represents a potential therapeutic strategy for HCC.
- ASPH-targeting antibodies may harness antiviral immunity for cancer treatment.
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