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Targeting CDCP1 boost CD8+ T cells-mediated cytotoxicity in cervical cancer via the JAK/STAT signaling pathway

Hua Huang1,2, Yuwen Pan1,2, Qiuwen Mai1,2

  • 1Department of Obstetrics and Gynecology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China.

Journal for Immunotherapy of Cancer
|October 25, 2024
PubMed
Abstract

Insights

Cervical cancer progression is linked to CUB domain-containing protein 1 (CDCP1) overexpression, which impairs T cell activity. Targeting CDCP1 with 8-prenylnaringenin (8PN) shows promise for enhancing antitumor immunity and improving patient outcomes.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Cervical cancer presents a significant global health burden.
  • Novel immunotherapeutic targets are crucial for advancing treatment strategies.

Purpose of the Study:

  • To investigate the role of CUB domain-containing protein 1 (CDCP1) in cervical cancer progression.
  • To evaluate CDCP1 as a potential therapeutic target for cervical cancer.

Main Methods:

  • Analysis of patient cohorts and preclinical models to correlate CDCP1 expression with prognosis.
  • Investigation of CDCP1's impact on the tumor immune microenvironment in mouse models, focusing on T cells (CTLs, Tregs).
  • Mechanistic studies on CDCP1's interaction with CD6 and JAK-STAT signaling.

Main Results:

  • CDCP1 overexpression correlates with poor prognosis and altered T cell activity (CTLs and Tregs) in cervical cancer.
  • CDCP1 binds to CD6, inhibiting T cell JAK-STAT signaling.
  • Inhibition of CDCP1 using 8-prenylnaringenin (8PN) suppressed tumor growth and boosted antitumor immunity in vivo.

Conclusions:

  • CDCP1 critically influences cervical cancer progression by modulating the tumor immune microenvironment.
  • Targeting CDCP1 represents a promising therapeutic strategy for improving cervical cancer patient outcomes.
Keywords:
Cervical CancerImmunotherapy

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