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Synthetic lethal genes to mutant p53

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  • 1. School of Life Science and Biotechnology, Kunming University of Science and Technology, Kunming 650500, China;
    2. Laboratory of Molecular Genetics of Aging and Tumor, Medical College of Kunming University of Science and Technology, Kunming 650500, China

Received date: 2014-08-18

  Online published: 2014-12-08

Abstract

Targeted therapy has become a powerful approach for cancer treatment. Better understanding of oncogenes as well as synthetic lethal interactions with oncogenes will lead to new strategies for tumor-specific treatment. It is well known that mutant p53 plays an important role in tumorigenesis and tumor development. Thus, understanding the synthetic lethal relationship between p53 mutations and interacting genes in tumor is critical for the personalized treatments of p53 mutant tumors. Synthetic lethal genes to mutant p53 can be divided into cell cycle regulators and non-cell cycle regulators. This paper review show these two types of target genes contribute to synthetic lethal interactions with p53 mutations and potential applications of these interactions in anticancer therapy.

Cite this article

Tongyang Liu,Haiqiang Guo,Meiyan Zhu,Yingze Huang,Shuting Jia,Ying Luo,Jihong Zhang . Synthetic lethal genes to mutant p53[J]. Hereditas(Beijing), 2015 , 37(4) : 321 -326 . DOI: 10.16288/j.yczz.14-277

References

[1] Dörr JR, Yu Y, Milanovic M, Beuster G, Zasada C, Däbritz JH, Lisec J, Lenze D, Gerhardt A, Schleicher K, Kratzat S, Pürfurst B, Walenta S, Mueller-Klieser W, Gräler M, Hummel M, Keller U, Buck AK, Dörken B, Willmitzer L, Reimann M, Kempa S, Lee S, Schmitt CA. Synthetic lethal metabolic targeting of cellular senescence in cancer therapy. Nature , 2013, 501(7467): 421-425.
[2] Chan DA, Giaccia AJ. Harnessing synthetic lethal interactions in anticancer drug discovery. Nat Rev Drug Discov , 2011, 10(5): 351-364.
[3] Pessetto ZY, Yan Y, Bessho T, Natarajan A. Inhibition of BRCT(BRCA1)-phosphoprotein interaction enhances the cytotoxic effect of olaparib in breast cancer cells: a proof of concept study for synthetic lethal therapeutic option. Breast Cancer Res Treat , 2012, 134(2): 511-517.
[4] Dietlein F, Thelen L, Jokic M, Jachimowicz RD, Ivan L, Knittel G, Leeser U, Van Oers J, Edelmann W, Heukamp LC, Reinhardt HC. A functional cancer genomics screen identifies a druggable synthetic lethal interaction between MSH3 and PRKDC . Cancer Discov , 2014, 4(5): 592-605.
[5] Warrener P, Kim S, Williams SM, Biery M, Gordon M, Toniatti C, Cleary MA, Linsley PS, Carleton M. Synthetic lethality of PARP inhibition in BRCA-network disrupted tumor cells is associated with interferon pathway activation and enhanced by interferon-γ. Apoptosis , 2012, 17(7): 691-701.
[6] Chan SL, Mok T. PARP inhibition in BRCA-mutated breast and ovarian cancers. Lancet , 2010, 376(9737): 211-213.
[7] Eliyahu D, Michalovitz D, Eliyahu S, Pinhasi-Kimhi O, Oren M. Wild-type p53 can inhibit oncogene-mediated focus formation. Proc Natl Acad Sci USA , 1989, 86(22): 8763-8767.
[8] Steele RJ, Lane DP. P53 in cancer: a paradigm for modern management of cancer. Surgeon , 2005, 3(3): 197-205.
[9] Nigro JM, Baker SJ, Preisinger AC, Jessup JM, Hostetter R, Cleary K, Bigner SH, Davidson N, Baylin S, Devilee P, Glover T, Collins FS, Weslon A, Modali R, Harris CC, Vogelstein B. Mutations in the p53 gene occur in diverse human tumour types. Nature , 1989, 342(6250): 705-708.
[10] Donehower LA, Harvey M, Slagle BL, Mcarthur MJ, Montgomery CA, Jr., Butel JS, Bradley A. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nature , 1992, 356(6366): 215-221.
[11] Vousden KH, Lu X. Live or let die: the cell's response to p53. Nat Rev Cancer , 2002, 2(8): 594-604.
[12] Liu J, Zhang C, Feng Z. Tumor suppressor p53 and its gain-of-function mutants in cancer. Acta Biochim Biophys Sin (Shanghai) , 2014, 46(3): 170-179.
[13] Kastan MB, Berkovich E. p53: a two-faced cancer gene. Nat Cell Biol , 2007, 9(5): 489-491.
[14] Dasika GK, Lin SC, Zhao S, Sung P, Tomkinson A, Lee EY. DNA damage-induced cell cycle checkpoints and DNA strand break repair in development and tumorigenesis. Oncogene , 1999, 18(55): 7883-7899.
[15] Wang Q, Fan S, Eastman A, Worland PJ, Sausville EA, O'connor PM. UCN-01: a potent abrogator of G2 checkpoint function in cancer cells with disrupted p53. J Natl Cancer Inst , 1996, 88(14): 956-965.
[16] Rowley R, Hudson J, Young PG. The wee1 protein kinase is required for radiation-induced mitotic delay. Nature , 1992, 356(6367): 353-355.
[17] Hirai H, Iwasawa Y, Okada M, Arai T, Nishibata T, Kobayashi M, Kimura T, Kaneko N, Ohtani J, Yamanaka K, Itadani H, Takahashi-Suzuki I, Fukasawa K, Oki H, Nambu T, Jiang J, Sakai T, Arakawa H, Sakamoto T, Sagara T, Yoshizumi T, Mizuarai S, Kotani H. Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents. Mol Cancer Ther , 2009, 8(11): 2992-3000.
[18] Wang Y, Decker SJ, Sebolt-Leopold J. Knockdown of Chk1, Wee1 and Myt1 by RNA interference abrogates G2 checkpoint and induces apoptosis. Cancer Biol Ther , 2004, 3(3): 305-313.
[19] Van Linden AA, Baturin D, Ford JB, Fosmire SP, Gardner L, Korch C, Reigan P, Porter CC. In
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