Extracellular matrix in prostate cancer anti-androgen resistance

Authors

  • Cheng-Bin Zhang Naval Medical University Author
  • Bin-Zhi Qian Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, The Human Phenome Institute, Zhangjiang-Fudan International Innovation Center, Fudan University, Shanghai 200438, China Author

DOI:

https://doi.org/10.17161/sjm.v2i2.23334

Keywords:

Prostate Cancer, ECM, ADT-resistance

Abstract

Extracellular matrix (ECM) within the tumour microenvironment (TME) of prostate cancer has been extensively reported to be associated with the development of androgen-deprivation therapy (ADT) resistance in prostate cancer. Recent-year investigations have illustrated that the deposition of ECM proteins contribute to this resistance by regulating cell behaviours of cancer cells directly or indirectly through modulating immune cells within the TME, thereby protecting cancer cells from the tumour-suppressing effects of ADT. Here we review these findings, offering new perspectives on prostate cancer research and highlighting the potential of ECM proteins as novel clinical targets for predicting and treating ADT-resistance.

Author Biography

  • Bin-Zhi Qian, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, The Human Phenome Institute, Zhangjiang-Fudan International Innovation Center, Fudan University, Shanghai 200438, China

    Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, The Human Phenome Institute, Zhangjiang-Fudan International Innovation Center, Fudan University, Shanghai 200438, China

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Published

03/20/2025

Issue

Vol. 2 No. 2 (2025)

Section

Review & Commentary

License

Copyright (c) 2025 Cheng-Bin Zhang, Bin-Zhi Qian (Author)

Creative Commons License

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

How to Cite

1.
Zhang CB, Qian BZ. Extracellular matrix in prostate cancer anti-androgen resistance. Serican J. Med. 2025;2(2). doi:10.17161/sjm.v2i2.23334