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Updated: Jun 18, 2025

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Trim21-mediated CCT2 ubiquitination suppresses malignant progression and promotes CD4+T cell activation in breast

Xi Chen1, Chenao Ma1, Yaming Li1

  • 1Department of Breast Surgery, General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.

Cell Death & Disease
|July 30, 2024
PubMed

Insights

Chaperone-dependent CCT2 protein promotes breast cancer growth and immune evasion. Its degradation by Trim21 and targeting CCT2 may offer new therapeutic strategies for breast cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Breast cancer progression and metastasis mechanisms require further elucidation.
  • Understanding the molecular drivers of breast cancer is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of CCT2 in breast cancer progression and metastasis.
  • To explore the underlying molecular mechanisms of CCT2's function.
  • To identify CCT2 as a potential therapeutic target and prognostic biomarker.

Main Methods:

  • Analysis of TCGA and GEO datasets for CCT2 expression.
  • Functional assays to assess CCT2's impact on tumor growth and metastasis.
  • Investigation of the JAK2/STAT3 signaling pathway.
  • Evaluation of Trim21's role in CCT2 regulation.
  • Analysis of exosomal CCT2 effects on CD4+ T cells and related signaling pathways.

Main Results:

  • CCT2 expression is significantly upregulated in breast cancer tissues and correlates with poor prognosis.
  • CCT2 promotes tumor growth and metastasis via JAK2/STAT3 pathway activation.
  • Trim21-mediated CCT2 degradation reverses protumorigenic effects.
  • Exosomal CCT2 suppresses CD4+ T cell activation and proinflammatory cytokine secretion by inhibiting Ca2+-NFAT1 signaling and reducing CD40L expression.

Conclusions:

  • CCT2 upregulation drives breast cancer progression and immune evasion.
  • CCT2 is a potential therapeutic target and prognostic predictor for breast cancer.
  • Targeting CCT2 or enhancing its degradation may represent a novel therapeutic strategy.

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