Macrophage/cancer cell interactions mediate hormone resistance by a nuclear receptor derepression pathway - PubMed (original) (raw)

. 2006 Feb 10;124(3):615-29.

doi: 10.1016/j.cell.2005.12.032.

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• PMID: 16469706
• DOI: 10.1016/j.cell.2005.12.032

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Macrophage/cancer cell interactions mediate hormone resistance by a nuclear receptor derepression pathway

Ping Zhu et al. Cell. 2006.

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Abstract

Defining the precise molecular strategies that coordinate patterns of transcriptional responses to specific signals is central for understanding normal development and homeostasis as well as the pathogenesis of hormone-dependent cancers. Here we report specific prostate cancer cell/macrophage interactions that mediate a switch in function of selective androgen receptor antagonists/modulators (SARMs) from repression to activation in vivo. This is based on an evolutionarily conserved receptor N-terminal L/HX7LL motif, selectively present in sex steroid receptors, that causes recruitment of TAB2 as a component of an N-CoR corepressor complex. TAB2 acts as a sensor for inflammatory signals by serving as a molecular beacon for recruitment of MEKK1, which in turn mediates dismissal of the N-CoR/HDAC complex and permits derepression of androgen and estrogen receptor target genes. Surprisingly, this conserved sensor strategy may have arisen to mediate reversal of sex steroid-dependent repression of a limited cohort of target genes in response to inflammatory signals, linking inflammatory and nuclear receptor ligand responses to essential reproductive functions.

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Comment in

• Inflammation and sex steroid receptors: a motif for change.
  Brosens JJ, Lam EW, Parker MG. Brosens JJ, et al. Cell. 2006 Feb 10;124(3):466-8. doi: 10.1016/j.cell.2006.01.023. Cell. 2006. PMID: 16469693

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