AI Article Synopsis
- HDAC3 is important for regulating gene transcription and is linked to cancer development, but how it is controlled in cancer is not well understood.
- This study found that PIWIL2 interacts with HDAC3, preventing its degradation and enhancing its activity, which is further boosted by CK2α.
- The research shows that PIWIL2 promotes cancer cell growth and reduces cell death by influencing HDAC3, providing new insights into its role in tumor development.
Article Abstract
HDAC3 is involved in deacetylation of histone and non-histone proteins, having a key role in the regulation of gene transcription and also in the process of tumorgenesis. However, how HDAC3 is regulated in cancer remains largely unclear. Here, we showed that PIWIL2 can interact with HDAC3, leading to stabilization of HDAC3 from ubiquitin-mediated degradation by competitive association with E3 ubiquitin ligase Siah2. Furthermore, we found that expression of PIWIL2 enhanced HDAC3 activity via CK2α. PIWIL2 facilitated the interaction between HDAC3 and CK2α, thus exhibiting a promotion on the HDAC3 phosphorylation by CK2α. Further work showed that PIWIL2 could promote cell proliferation and suppress cell apoptosis via regulating HDAC3. Our present study firstly revealed that PIWIL2 can play a role in HDAC3-mediated epigenetic regulation on cancer cell proliferation and apoptosis. These findings provide a novel insight into the roles of PIWIL2 in tumorigenesis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5859188 | PMC |
| http://dx.doi.org/10.1038/s41419-018-0462-8 | DOI Listing |
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