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Role of phosphorylation of p53 at Ser392 in cancer therapy
LIU Jing-li SHI Xin-li CUI Cheng REN Lai-feng ZHENG Wen-guang LI Ming-yuan*
Acta Anatomica Sinica ›› 2014, Vol. 45 ›› Issue (3) : 437-440.
Role of phosphorylation of p53 at Ser392 in cancer therapy
Phosphorylation is the most common way of p53 post-translational modifications. However, gaps still exist in our knowledge regarding the role and mechanism of phosphorylation of p53 at Ser392 in carcinogenesis and cancer prevention. In the present study, we summarized the effect of phos-p53-Ser392 to wild-type and mutant p53, the regulation by DNA damage agents and protein kinase, and the significance of phosphorylation of p53-Ser392 in cancer treatment.
p53 / Ser392 / Phosphorylation / Cancer therapy / Gene mutant / Western blotting
［1］Wade M, Li Y-C, Wahl GM. MDM2, MDMX and p53 in oncogenesis and cancer therapy［J］. Nature Reviews Cancer, 2013, 13(2):83-96.
［2］Retzlaff M, Rohrberg J, Küpper NJ, et al. The regulatory domain stabilizes the p53 tetramer by intersubunit contacts with the DNA binding domain［J］. J Mol Biol,2013, 425(1,9):144-155.［3］Kim YY, Park BJ, Kim DJ, et al. Modification of serine 392 is a critical event in the regulation of p53 nuclear export and stability［J］. FEBS Letters, 2004, 572(1):92-98.
［4］Loughery J, Meek D. Switching on p53: an essential role for protein phosphorylation［J］. Bio Discov, 2013, 8(1):1-20.
［5］Ashcroft M, Kubbutat MH, Vousden KH. Regulation of p53 function and stability by phosphorylation［J］. Mol Cell Biol, 1999, 19(3):1751-1758.
［6］Thompson T, Tovar C, Yang H, et al. Phosphorylation of p53 on key serines is dispensable for transcriptional activation and apoptosis［J］. J Biol Chem, 2004, 279(51):53015-53022.
［7］Hao M, Lowy AM, Kapoor MD, et al. Mutation of phosphoserine 389 affects p53 function in vivo［J］. J Biol Chem, 1996, 271(46):29380-29385.
［8］Muller PA, Vousden KH. p53 mutations in cancer［J］. Nat Cell Biol, 2013, 15(1):2-8.
［9］Li HZh, Yu K,Wang ZM,et al.The relationships between parameters of cell kinetics and expression, mutation of related genes in breast cancer［J］. Acta Anatomica Sinica, 2003, 34(4): 390-394. (in Chinese)
李红智, 俞康,王宗敏，等.乳腺癌细胞动力学指标与相关基因表达、突变的关系［J］. 解剖学报, 2003, 34(4): 390-394.
［10］Yap DBS, Hsieh JK, Zhong S, et al.Ser392 phosphorylation regulates the oncogenic function of mutant p53［J］. Cancer Research, 2004, 64(14):4749-4754.
［11］Gillotin S, Yap D, Lu X. Mutation at Ser392 specifically sensitizes mutant p53H175 to mdm2mediated degradation［J］. Cell Cycle, 2010, 9(7):1390-1398.
［12］Fan G, Ma X, Wong P, et al. p53 dephosphorylation and p21Cip1/Waf1 translocation correlate with caspase-3 activation in TGF-β1-induced apoptosis of HuH7 cells［J］. Apoptosis, 2004, 9(2):211-221.
[13］Cox ML, Meek DW. Phosphorylation of serine 392 in p53 is a common and integral event during p53 induction by diverse stimuli［J］. Cell Signal, 2010, 22(3):564-571.
［14］Blaydes JP, Hupp TR. DNA damage triggers DRB-resistant phosphorylation of human p53 at the CK2 site［J］. Oncogene, 1998, 17(8):1045-1052.
［15］Bode AM, Dong Z. Post-translational modification of p53 in tumorigenesis［J］. Nat Rev Cancer, 2004, 4(10):793-805.
［16］Meek DW. Multisite phosphorylation and the integration of stress signals at p53［J］. Cell Signal, 1998, 10(3):159-166.
［17］Lew QJ, Chia YL, Chu KL, et al.Identification of HEXIM1 as a positive regulator of p53［J］. J Biol Chem, 2012, 287(43):36443-36454.
［18］Lew QJ, Chu KL, Chia YL, et al. HEXIM1, a new player in the p53 pathway［J］. Cancers, 2013, 5(3):838-856.
［19］Matsumoto M, Furihata M, Kurabayashi A, et al. Prognostic significance of serine 392 phosphorylation in overexpressed p53 protein in human esophageal squamous cell carcinoma［J］. Oncology, 2004, 67(2):143-150.
［20］Bar JK, Slomska I, Rabczynki J, et al. Expression of p53 protein phosphorylated at serine 20 and serine 392 in malignant and benign ovarian neoplasms: correlation with clinicopathological parameters of tumors［J］. Int J Gynecol Cancer, 2009, 19(8):1322-1328.
［21］Kapoor NR, Ahuja R, Shukla SK, et al. The HBx protein of hepatitis B virus confers resistance against nucleolar stress and anti-cancer drug-induced p53 expression［J］. FEBS Letters, 2013, 587(9):1287-1292.
［22］Kofod-Olsen E, M?ller JM, Schleimann MH, et al. Inhibition of p53-dependent, but not p53-independent, cell death by U19 protein from human herpesvirus 6B［J］. PloS One, 2013, 8(3):e59223.
［23］Pise-Masison CA, Radonovich M, Sakaguchi K, et al. Phosphorylation of p53: a novel pathway for p53 inactivation in human T-cell lymphotropic virus type 1-transformed cells［J］. J Virol, 1998, 72(8):6348-6355.
［24］Mukerjee R, Claudio PP, Chang JR, et al. Transcriptional regulation of HIV-1 gene expression by p53［J］. Cell Cycle, 2010, 9(22):4569-4578.
［25］Zhang J, Biggar KK, Storey KB. Regulation of p53 by reversible post-transcriptional and post-translational mechanisms in liver and skeletal muscle of an anoxia tolerant turtle, Trachemys scripta elegans ［J］. Gene, 2013, 513(1):147-155.
［26］Aboudehen K, Hilliard S, Saifudeen Z, et al. Mechanisms of p53 activation and physiological relevance in the developing kidney［J］. Am J Physiol Renal Physiol, 2012, 302(8):928-940.
［27］Flores-López LA, Díaz-Flores M, García-Macedo R, et al. High glucose induces mitochondrial p53 phosphorylation by p38 MAPK in pancreatic RINm5F cells［J］. Molecular Biol Rep, 2013, 40(8):4947-4958.
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