Abstract:
:We investigated the effect of HMGB2 on the stability of p53 protein in HeLa cells. Overexpression of HMGB2 led to accumulation of the p53 protein, whereas HMGB2 knockdown with siRNA resulted in a substantial decrease in the p53 protein level. The HMGB2-dependent increase of p53 stability was specific for HPV-positive HeLa cells as HCT116 and MCF7 cell lines did not demonstrate this response. Co-expression of HMGB2 and HPV E6 prevented HPV E6 protein-mediated ubiquitination and degradation of p53. FACS analysis exhibited that HeLa cells transfected with HMGB2 displayed decreased cell proliferation, with a concomitant increase of the p53 protein and arrest of the cell cycle, predominantly in G1 phase. Our findings collectively suggest that HMGB2 could stabilize p53 by interfering with E6/E6AP-mediated p53 degradation in HPV-positive HeLa cells.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Lee D,Kwon JH,Kim EH,Kim ES,Choi KYdoi
10.1016/j.canlet.2009.11.015subject
Has Abstractpub_date
2010-06-01 00:00:00pages
125-32issue
1eissn
0304-3835issn
1872-7980pii
S0304-3835(09)00685-5journal_volume
292pub_type
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