AI Article Synopsis

  • Dioscin shows promise as an anticancer agent against prostate cancer (PCa), but its mechanism of action is not fully understood.
  • The study indicates that dioscin may inhibit PCa growth by targeting the SHP1 protein, leading to increased SHP1 phosphorylation and disruption of the P38 signaling pathway.
  • Dioscin also promotes apoptosis in PCa cells, suggesting its potential as a future treatment for both androgen-sensitive and androgen-independent forms of the disease.

Article Abstract

Dioscin possesses antioxidant effects and has anticancer ability in many solid tumors including prostate cancer (PCa). Nevertheless, its effect and mechanism of anti-PCa action remain unclear. The tyrosine protein phosphatase SHP1, which contains an oxidation-sensitive domain, has been confirmed as a target for multicancer treatment. Further studies are needed to determine whether dioscin inhibits PCa through SHP1. We performed studies using androgen-sensitive (LNCaP) and androgen-independent (LNCaP -C81) cells to investigate the anticancer effects and possible mechanisms of dioscin after administering interleukin-6 (IL-6) and dihydrotestosterone (DHT). Our results show that dioscin inhibited cell growth and invasion by increasing SHP1 phosphorylation [p-SHP1 (Y536)] and inhibiting the subsequent P38 mitogen-activated protein kinase signaling pathway. Further studies confirmed that dioscin promoted caspase-3 and Bad-related cell apoptosis in these two cell lines. Our research suggests that the anticancer effects of dioscin on PCa may occur through SHP1. Dioscin may be useful to treat androgen-sensitive and independent PCa in the future.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7394018PMC
http://dx.doi.org/10.3389/fphar.2020.01099DOI Listing

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