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Active regulator of SIRT1 is required for cancer cell survival but not for SIRT1 activity. | LitMetric

AI Article Synopsis

  • SIRT1 is a deacetylase linked to various cellular processes and negatively correlates with cancer survival; AROS is the first identified post-transcriptional regulator enhancing SIRT1 activity and its impact on the p53 protein.
  • Research indicates that AROS affects p53 acetylation differently depending on the cell type, suppressing it primarily under stress conditions, while SIRT1 consistently suppresses p53 across various conditions.
  • Knocking down AROS leads to apoptosis in cancer cells independently of p53 activation, suggesting that AROS may play a critical role in promoting cancer cell survival without being necessary for the viability of non-cancer cells.

Article Abstract

The NAD(+)-dependent deacetylase SIRT1 is involved in diverse cellular processes, and has also been linked with multiple disease states. Among these, SIRT1 expression negatively correlates with cancer survival in both laboratory and clinical studies. Active regulator of SIRT1 (AROS) was the first reported post-transcriptional regulator of SIRT1 activity, enhancing SIRT1-mediated deacetylation and downregulation of the SIRT1 target p53. However, little is known regarding the role of AROS in regulation of SIRT1 during disease. Here, we report the cellular and molecular effects of RNAi-mediated AROS suppression, comparing this with the role of SIRT1 in a panel of human cell lines of both cancerous and non-cancerous origins. Unexpectedly, AROS is found to vary in its modulation of p53 acetylation according to cell context. AROS suppresses p53 acetylation only following the application of cell damaging stress, whereas SIRT1 suppresses p53 under all conditions analysed. This supplements the original characterization of AROS but indicates that SIRT1 activity can persist following suppression of AROS. We also demonstrate that knockdown of AROS induces apoptosis in three cancer cell lines, independent of p53 activation. Importantly, AROS is not required for the viability of three non-cancer cell lines indicating a putative role for AROS in specifically promoting cancer cell survival.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3843821PMC
http://dx.doi.org/10.1098/rsob.130130DOI Listing

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