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Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment

Wen-Jye Lin1, Kouji Izumi2

  • 1Immunology Research Center; National Health Research Institutes; Zhunan, Taiwan.

Oncoimmunology
|October 24, 2014
PubMed

Insights

Inhibiting the androgen receptor (AR) in prostate cancer paradoxically increases CCL2, promoting metastasis via STAT3 activation. This suggests AR inhibition alone is insufficient for effective prostate cancer treatment.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • High chemokine (C-C motif) ligand 2 (CCL2) levels drive prostate cancer metastasis by recruiting macrophages.
  • Androgen receptor (AR) signaling is a key target in prostate cancer therapy.

Purpose of the Study:

  • To investigate the impact of androgen receptor (AR) inhibition on CCL2 expression and prostate cancer progression.
  • To elucidate the mechanisms by which AR inhibition influences tumor microenvironment and metastasis.

Main Methods:

  • Studied the effects of AR inhibition in prostate cancer cells and tumor-infiltrating macrophages.
  • Analyzed CCL2 upregulation, signal transducer and activator of transcription 3 (STAT3) activation, and epithelial-to-mesenchymal transition (EMT).

Main Results:

  • AR inhibition in prostate cancer cells or macrophages upregulated CCL2.
  • CCL2 upregulation promoted disease progression by activating STAT3.
  • AR inhibition favored epithelial-to-mesenchymal transition, a key process in metastasis.

Conclusions:

  • Sole inhibition of the androgen receptor (AR) is insufficient for effective prostate cancer therapy.
  • AR inhibition can inadvertently promote prostate cancer metastasis through CCL2/STAT3 pathway activation.
  • Combined therapeutic strategies may be necessary to overcome resistance to AR-targeted therapies.
Keywords:
CCL2STAT3androgen receptorepithelial-to-mesenchymal transitionprostate cancer

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