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- Title
TOR4A suppresses HPV16-related cervical cancer invasion and metastasis through Treg depletion.
- Authors
Qing Zhang; Qiuli Teng; Xinyue Ma; Peihui Wang; Beihua Kong
- Abstract
Objective: Cervical cancer is a prominent affliction among women, primarily attributed to high-risk human papillomavirus (HPV) infection and its consequential cervical lesions. This study endeavors to elucidate the underlying mechanisms involved in the malignant transformation of the cervix induced by HPV, with a specific emphasis on the identification and characterization of proteins that interact with HPV16. Methods: Utilizing BioID protein-protein interaction technology, we investigated the interaction mechanisms between HPV16 and TOR4A. Employing a humanized cervical mouse model, we conducted mass cytometry analysis to explore the immune microenvironment. This allowed us to examine the impact of TOR4A on the immune microenvironment and delve deeper into the underlying mechanisms. Results: Our findings revealed that HPV16 disrupts the tumorsuppressive function of TOR4A, leading to compensatory upregulation of TOR4A expression. Mass cytometry were employed to observe TOR4A's role in inhibiting Treg cell depletion, thereby contributing to immune activation. This immune modulation by TOR4A subsequently suppressed cervical cancer proliferation and metastasis. Conclusion: The results of our study indicate that HPV16 interferes with the tumor-suppressive activity of TOR4A, resulting in an increase in TOR4A expression as a compensatory response. To investigate the involvement of TOR4A in inhibiting Treg cell depletion and its contribution to immune activation, we employed mass cytometry techniques. The observed immune modulation by TOR4A subsequently led to the suppression of cervical cancer proliferation and metastasis.
- Subjects
CERVICAL cancer; METASTASIS; REGULATORY T cells; HUMAN papillomavirus; IMMUNOREGULATION; GENITAL warts
- Publication
Journal of Gynecologic Oncology, 2024, Vol 35, p28
- ISSN
2005-0380
- Publication type
Article
- DOI
10.3802/jgo.2024.35.S2.P15