SPOP is essential for DNA replication licensing through maintaining translation of CDT1 and CDC6 in HaCaT cells

In this study, we evaluated the cellular functions of wild-type SPOP in non-cancerous human keratinocyte-derived HaCaT cells expressing wild-type SPOP gene. SPOP knockdown using siRNA in HaCaT cells dramatically reduced cell growth and arrested their cell cycles at G1/S phase. The expression of DNA replication licensing factors CDT1 and CDC6 in HaCaT cells drastically decreased on SPOP knockdown as their translation was inhibited. CDT1 and CDC6 downregulation induced p21 expression without p53 activation. Our results suggest that SPOP is essential for DNA replication licensing in non-cancerous keratinocyte HaCaT cells.PMID:36791496 | DOI:10.1016/j.bbrc.2023.02.012

Source: Biochemical and Biophysical Research communications - February 15, 2023 Category: Biochemistry Authors: Sayoko Sanada Masashi Maekawa Sota Tate Hiroki Nakaoka Yasuhiro Fujisawa Koji Sayama Shigeki Higashiyama Source Type: research