Home Neoplasma 2021 Neoplasma Vol.68, No.1, p.119–125, 2021

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Neoplasma Vol.68, No.1, p.119–125, 2021

Title: CacyBP/SIP protein reduces p53 stability by enhancing Mdm2 activity in p53 mutant glioma cells
Author: Fengyuan Qian, Tianjin Tang, Shiquan Wang, Bin Wang, Lei Wang, Hengliang Shi

Abstract: Our previous studies have illustrated that CacyBP/SIP (Calcyclin-binding protein or Siah-1-interacting protein) promoted the proliferation of glioma cells. However, the possible mechanism still needs to be clarified. In the current study, we aimed to uncover the potential mechanism of CacyBP/SIP in regulating glioma cell proliferation. We found that CacyBP/SIP decreased the protein level of p53, but not the mRNA level of p53 in p53 mutant U251 cell line, whereas, in p53 wild-type U87 cell line, CacyBP/SIP neither promoted its proliferation nor regulated the changes of p53 protein. Further investigation indicated that CacyBP/SIP interacted with p53 and Mdm2 (Mouse double minute 2) to promote p53 ubiquitination and subsequent proteasome-mediated degradation in U251. Moreover, in the presence of Mdm2, CacyBP/SIP boosted the ubiquitination of p53 in a dose-dependent manner. On the contrary, inhibition of Mdm2 activity significantly increased the stability of p53. Finally, we found that the protein level of CacyBP/SIP and p53 is inversely correlated in p53 mutant human glioma tissues. These observations suggest an underlying mechanism that CacyBP/SIP promotes the degradation of p53 by enhancing Mdm2 E3 ligase activity, which reveals a novel pathway for the regulation of mutant p53 and provides a new therapeutic approach to target the CacyBP/SIP-induced glioma cell proliferation.

Keywords: CacyBP/SIP; p53; Mdm2; glioma; tumorigenesis
Published online: 03-Sep-2020
Year: 2021, Volume: 68, Issue: 1 Page From: 119, Page To: 125
doi:10.4149/neo_2020_200414N399
Price: 16.80 €






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