Experimental and Molecular Medicine (Jul 2018)

ARD1/NAA10 acetylation in prostate cancer

  • Katherine J. Kuhns,
  • Guanyi Zhang,
  • Zehua Wang,
  • Wanguo Liu

DOI
https://doi.org/10.1038/s12276-018-0107-0
Journal volume & issue
Vol. 50, no. 7
pp. 1 – 8

Abstract

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Prostate cancer: Preventing androgen receptor activation Blocking the addition of an acetyl group to androgen receptors by Arrest-defect-1 protein (ARD1) might be an effective strategy for halting prostate cancer progression. High levels of ARD1 are found in many types of cancer and previous studies have shown that it contributes to prostate cancer (PCa) cell proliferation and survival by stimulating androgen receptor activity. Wanguo Liu and colleagues at Louisiana State University Health Sciences Center, New Orleans, USA, review current knowledge of the regulation and effects of ARD1 on tumor formation. The ARD1-mediated post-translational modification of androgen receptors causes them to move from the cytoplasm to the nucleus where they activate the expression of genes involved in tumor growth. Compounds that inhibit this modification could offer a new treatment option for patients with prostate cancer.