Premium
The tumor suppressor p33 ING1b upregulates p16 INK4a expression and induces cellular senescence
Author(s) -
Li Na,
Li Qian,
Cao Xiaoxiao,
Zhao Ganye,
Xue Lixiang,
Tong Tanjun
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.08.044
Subject(s) - senescence , cellular senescence , suppressor , chemistry , tumor suppressor gene , cancer research , biology , microbiology and biotechnology , gene , carcinogenesis , biochemistry , phenotype
ING1 protein is a tumor suppressor which plays significant roles in multiple cellular activities. p47 ING1a and p33 ING1b are major splice isoforms of ING1 and their roles in senescence need further investigations. Here we studied the functions of ING1 isoforms in cellular senescence and gene regulation, with focus on p16 INK4a . We observe that p33 ING1b protein is the major ING1 isoform expressed in 2BS human diploid fibroblasts. Overexpression of p33 ING1b induces cellular senescence and upregulates p16 INK4a expression in 2BS fibroblasts. p33 ING1b upregulates p16 INK4a transcription. p33 ING1b and p300 bind to the p16 INK4a promoter. p300/CBP‐specific inhibitor curcumin can reverse the induction of p16 INK4a by p33 ING1b . These results help to better understand the function of ING1.