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  1. Home
  2. Research Domains
  3. Biomedical And Clinical Sciences
  4. Oncology And Carcinogenesis
  5. Predictive And Prognostic Markers
  6. Cdcp1 Overexpression Drives Prostate Cancer Progression And Can Be Targeted In Vivo.

CDCP1 overexpression drives prostate cancer progression and can be targeted in vivo.

Abdullah Alajati1,2, Mariantonietta D'Ambrosio1,2,3, Martina Troiani1,2

  • 1Institute of Oncology Research (IOR), Oncology Institute of Southern Switzerland (IOSI), Bellinzona, Switzerland.

The Journal of Clinical Investigation
|April 7, 2020

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View abstract on PubMed

Summary
This summary is machine-generated.

Castration-resistant prostate cancer (CRPC) progression is driven by CUB domain-containing protein 1 (CDCP1) overexpression, especially with PTEN loss. Targeting CDCP1 offers new therapeutic strategies for metastatic prostate tumors.

Keywords:
OncologyProstate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Prostate cancer's transition to castration-resistant prostate cancer (CRPC) is poorly understood.
  • Identifying genetic alterations driving CRPC is crucial for developing new therapies.
  • CUB domain-containing protein 1 (CDCP1) is a transmembrane protein implicated in cancer progression.

Purpose of the Study:

  • To investigate the role of CDCP1 in the development of CRPC.
  • To identify mechanisms linking CDCP1 to prostate cancer metastasis.
  • To explore therapeutic strategies targeting CDCP1 in metastatic prostate cancer.

Main Methods:

  • Analysis of CDCP1 expression in CRPC patient samples.
  • Investigating the interaction between CDCP1, PTEN loss, and androgen signaling.
  • Utilizing anti-CDCP1 immunoliposomes (anti-CDCP1 ILs) in combination with enzalutamide for treatment studies.

Main Results:

  • CDCP1 is overexpressed in a subset of CRPC and cooperates with PTEN loss to promote metastasis.
  • Androgen deprivation combined with PTEN loss upregulates CDCP1, activating the SRC/MAPK pathway.
  • Anti-CDCP1 ILs loaded with chemotherapy suppressed tumor growth when combined with enzalutamide.

Conclusions:

  • CDCP1 is a significant driver of prostate cancer progression to the metastatic CRPC stage.
  • The interplay between androgens, PTEN, and CDCP1 is a key mechanism in CRPC development.
  • Targeting CDCP1, potentially with immunoliposomes and chemotherapy, presents a viable therapeutic approach for metastatic prostate cancer.