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Isolation, Culture, and Characterization of Prostate Cancer-Associated Fibroblasts
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CCT2 Promotes Prostate Cancer Progression Through EIF3F-Dependent Stabilization of FASN.

Shun Xu1,2,3, Yifan Zhang1,2,3, Haolin Li4

  • 1Department of Urology, the First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|June 3, 2026
PubMed
Summary
This summary is machine-generated.

Chaperonin-containing TCP1 subunit 2 (CCT2) drives prostate cancer by stabilizing fatty acid synthase (FASN), promoting lipid synthesis. Targeting the CCT2-EIF3F-FASN axis offers a novel therapeutic strategy for metabolic intervention in prostate cancer.

Keywords:
CCT2EIF3FFASNlipid metabolism reprogrammingprostate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Prostate cancer (PCa) progression is linked to altered lipid metabolism.
  • Fatty acid synthase (FASN) is upregulated in PCa, but its regulation and role in oncogenic lipid metabolism are not fully understood.

Purpose of the Study:

  • To identify key regulators of FASN stability and function in prostate cancer.
  • To elucidate the mechanisms by which these regulators promote PCa progression.
  • To evaluate potential therapeutic targets within this regulatory axis.

Main Methods:

  • Identified CCT2 as an oncogenic regulator using in vitro and in vivo models.
  • Investigated the transcriptional regulation of CCT2 by FOXA1.
  • Characterized the interaction between CCT2, EIF3F, and FASN to form a ternary complex.
  • Assessed the impact of FASN inhibition (orlistat) and CCT2-EIF3F disruption (Y043-8015) on tumor progression.
  • Evaluated combined therapeutic effects in isograft and patient-derived xenograft models.

Main Results:

  • CCT2 promotes lipid synthesis and enhances malignant phenotypes in PCa.
  • CCT2 transcription is upregulated by FOXA1.
  • CCT2, EIF3F, and FASN form a complex that enhances FASN deubiquitination and stability, increasing lipid synthesis.
  • Inhibition of FASN or disruption of the CCT2-EIF3F interaction suppressed tumor progression.
  • Combined treatment demonstrated synergistic antitumor effects, reducing tumor growth and metastasis.

Conclusions:

  • CCT2 is a critical regulator of lipid metabolism in prostate cancer, promoting tumor progression by stabilizing FASN via interaction with EIF3F.
  • The CCT2-EIF3F-FASN axis represents a promising therapeutic target for metabolic intervention in PCa.
  • Combined inhibition strategies targeting FASN and the CCT2-EIF3F interaction show significant potential for synergistic antitumor effects.