CTHRC1 expresses in cancer-associated fibroblasts and is associated with resistance to anti-androgen therapy in prostate cancer

  • 0Department of Urology, The First Affiliated Hospital of Guangxi Medical University, 6 Shuangyong Road, Nanning, 530021, China.

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Summary

This summary is machine-generated.

High CTHRC1 expression in prostate cancer correlates with poorer prognosis and resistance to anti-androgen therapy (ADT). Targeting CTHRC1 may offer new diagnostic and therapeutic strategies for prostate cancer treatment.

Area Of Science

  • Oncology
  • Molecular Biology
  • Genomics

Background

  • CTHRC1 is overexpressed in prostate cancer, promoting cell proliferation, invasion, and migration.
  • The precise role of CTHRC1 in prostate cancer prognosis and treatment outcomes is not well understood.

Purpose Of The Study

  • To investigate the expression patterns of CTHRC1 in prostate cancer.
  • To elucidate the functional significance of CTHRC1 in prostate cancer progression.
  • To evaluate the prognostic value and therapeutic implications of CTHRC1.

Main Methods

  • Utilized bulk and single-cell RNA sequencing on 1999 prostate cancer cases and 531 controls.
  • Analyzed CTHRC1 expression, prognostic correlations, and immune cell infiltration using CIBERSORT.
  • Predicted drug sensitivity to anti-androgen therapy (ADT) using the GDSC database.

Main Results

  • CTHRC1 expression is elevated in prostate cancer and increases with disease progression.
  • Higher CTHRC1 levels are associated with a worse progression-free interval (PFI) and increased tumor-associated macrophage (TAM) infiltration.
  • CTHRC1-positive myofibroblast-like cancer-associated fibroblasts (myCAFs) activate TGF-β signaling and are linked to ADT resistance, potentially via the CCN2/CAV1/AR pathway.

Conclusions

  • CTHRC1 is a significant risk factor for prostate cancer progression.
  • CTHRC1 expression in myCAFs influences the tumor microenvironment and hormone response.
  • CTHRC1 represents a potential therapeutic target for overcoming ADT resistance in prostate cancer.

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