Abstract:
:The known members of inhibitor of growth (ING) gene family are considered as candidate tumor suppressor genes. ING4, a novel member of ING family, is recently reported to interact with tumor suppressor p53, p300 (a major component of histone acetyl transferase complexes), and p65(RelA) subunit of NF-kappaB. In this study, we investigated the cellular behaviors of HepG2 cells with exogenous ING4. Interestingly, the overexpression of ING4 negatively regulated the cell growth with significant G2/M arrest of cell cycle, and moreover, enhanced the cell apoptosis triggered by serum starvation in HepG2 cells. Furthermore, the exogenous ING4 could upregulate endogenous p21 and Bax in HepG2 cells, not in p53-deficient Saos-2 cells, suggesting that G2/M arrest induced by ING4 could be mediated by the increased p21 expression in a p53-dependent manner, although there is no significant increase of p53 expression in HepG2 cells. Moreover, HepG2 cells with exogenous ING4 could significantly increase cell death, as exposed to some DNA-damage agents, such as etoposide and doxorubicin, implying that ING4 could enhance chemosensitivity to certain DNA-damage agents in HepG2 cells.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Zhang X,Xu LS,Wang ZQ,Wang KS,Li N,Cheng ZH,Huang SZ,Wei DZ,Han ZGdoi
10.1016/j.febslet.2004.06.010keywords:
subject
Has Abstractpub_date
2004-07-16 00:00:00pages
7-12issue
1-3eissn
0014-5793issn
1873-3468pii
S0014579304007276journal_volume
570pub_type
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