@2024 Afarand., IRAN
ISSN: 2252-0805 The Horizon of Medical Sciences 2014;20(3):191-201
ISSN: 2252-0805 The Horizon of Medical Sciences 2014;20(3):191-201
Role of p53 in Apoptosis and Cancer Therapy
ARTICLE INFO
Article Type
Analytic ReviewAuthors
Noori-Daloii M.R. (* )Abdollahzade R. (1 )
(* ) Medical Genetics Department, Medicine Faculty, Tehran University of Medical sciences, Tehran, Iran
(1 ) Medical Genetics Department, Medicine Faculty, Tehran University of Medical sciences, Tehran, Iran
Correspondence
Address: No. 24, Raja’ei 13th, Raja’ei Street, Ferdows, South Khorasan, Iran. Postal Code: 9771996136Phone: +985342222801
Fax: +985342222806
m35tabey@gmail.com
Article History
Received: August 3, 2014Accepted: September 5, 2014
ePublished: September 23, 2014
ABSTRACT
Conclusion
Due to the vital roles of P53 in carcinogenesis inhibition, this protein is one of
the most important therapeutic targets for cancer therapy. Based on genetic variation type in
P53, in the normal and tumor cells, a combination of different therapies can be used and also
by more comprehensive consideration of the involved signaling pathways new upstream and
downstream novel proteins can be discovered to act as targets for new therapeutic targets.
CITATION LINKS
[1]Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000;100(1):57-70.
[2]Noori-Daloii MR. Medical molecular genetics in the third millennium. Tehran: Nashr-e-akhar; 2009. [Persian]
[3]Turnpenny PD, Ellard S. Principles of medical genetics Emery’s elements of medical genetics. Noori Daloii MR (Translator). 14th ed. Tehran: Jame’e Negar; 2012. [Persian]
[4]Lane DP, Crawford LV. T antigen is bound to a host protein in SY40-transformed cells. Nature. 1979;278:261-3.
[5]Baker SJ, Fearon ER, Nigro JM, Hamilton SR, Preisinger AC, Jessup JM, et al. Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas. Science. 1989;244(4901):217-21.
[6]Finlay CA, Hinds PW, Levine AJ. The p53 proto-oncogene can act as a suppressor of transformation. Cell. 1989;57(7):1083-93.
[7]Vazquez A, Bond EE, Levine AJ, Bond GL. The genetics of the p53 pathway, apoptosis and cancer therapy. Nat Rev Drug Discov. 2008;7(12):979-87.
[8]Vogelstein B, Lane D, Levine AJ. Surfing the p53 network. Nature. 2000;408(6810):307-10.
[9]Dornan D, Wertz I, Shimizu H, Arnott D, Frantz GD, Dowd P, et al. The ubiquitin ligase COP1 is a critical negative regulator of p53. Nature. 2004;429(6987):86-92.
[10]Leng RP, Lin Y, Ma W, Wu H, Lemmers B, Chung S, et al. Pirh2, a p53-induced ubiquitin-protein ligase, promotes p53 degradation. Cell. 2003;112(6):779-91.
[11]Bullock AN, Henckel J, Fersht AR. Quantitative analysis of residual folding and DNA binding in mutant p53 core domain: Definition of mutant states for rescue in cancer therapy. Oncogene. 2000;19(10):1245-56.
[12]Noori-Daloii MR, Yaghoubi MM. Apoptosis or programmed cell death and cancer. Tehran: 6th Razi Conference of Medical Sciences; 2000. [Persian]
[13]Noori-Daloii MR, Vand Rajabpour F. Roles of miRNAs in gene expression regulation, apoptosis, diagnosis and treatment of cancer. Med Sci J Islamic Azad Univ Tehran Med Branch. 2011;21(3):151-161. [Persian]
[14]Tiwari M. Apoptosis, angiogenesis and cancer therapies. J Cancer Ther Res. 2012;1(1):3.
[15]Carmeliet P. Angiogenesis in health and disease. Nat Med. 2003;9(6):653-60.
[16]Sharma MR, Tuszynski GP, Sharma MC. Angiostatin-induced inhibition of endothelial cell proliferation/apoptosis is associated with the down-regulation of cell cycle regulatory protein cdk5. J Cell Biochem. 2004;91(2):398-409.
[17]Browder T, Folkman J, Pirie-Shepherd S. The hemostatic system as a regulator of angiogenesis. J Biol Chem. 2000;275(3):1521-4.
[18]Jiang L, Sheikh MS, Huang Y. Decision making by p53: Life versus death. Mol Cell Pharmacol. 2010;2(2):69-77.
[19]Sridhar SS, Shepherd FA. Targeting angiogenesis: A review of angiogenesis inhibitors in the treatment of lung cancer. Lung Cancer. 2003;42 Suppl 1:S81-91.
[20]Kelly PN, Strasser A. The role of Bcl-2 and its pro-survival relatives in tumourigenesis and cancer therapy. Cell Death Differ. 2011;18(9):1414-24.
[21]Kim K, Jeong KW, Kim H, Choi J, Lu W, Stallcup MR, et al. Functional interplay between p53 acetylation and H1. 2 phosphorylation in p53-regulated transcription. Oncogene. 2012;31(39):4290-301.
[22]Nicholls P, Mason MG, Cooper CE. Cytochrome c oxidase heme and Cu centres: Redox and spectral interactions. Biochimica et Biophysica Acta (BBA)-Bioenergetics. 2012;1817:S111.
[23]Manzl C, Fava L, Krumschnabel G, Peintner L, Tanzer M, Soratroi C, et al. Death of p53-defective cells triggered by forced mitotic entry in the presence of DNA damage is not uniquely dependent on Caspase-2 or the PIDDosome. Cell Death Disease. 2013;4(12):e942.
[24]Dorstyn L, Puccini J, Wilson C, Shalini S, Nicola M, Moore S, et al. Caspase-2 deficiency promotes aberrant DNA-damage response and genetic instability. Cell Death Differ. 2012;19(8):1288-98
[25]El-Deiry WS. The role of p53 in chemosensitivity and radiosensitivity. Oncogene. 2003;22(47):7486-95.
[26]Lowe SW, Bodis S, McClatchey A, Remington L, Ruley HE, Fisher DE, et al. p53 status and the efficacy of cancer therapy in vivo. Science. 1994;266(5186):807-10.
[27]Lu C, El-Deiry WS. Targeting p53 for enhanced radio- and chemo-sensitivity. Apoptosis. 2009;14(4):597-606.
[28]Williams JR, Zhang Y, Zhou H, Gridley DS, Koch CJ, Russell J, et al. A quantitative overview of radiosensitivity of human tumor cells across histological type and TP53 status. Int J Radiat Biol. 2008;84(4):253-64.
[29]Bertheau P, Plassa F, Espié M, Turpin E, de Roquancourt A, Marty M, et al. Effect of mutated TP53 on response of advanced breast cancers to high-dose chemotherapy. Lancet. 2002;360(9336):852-4.
[30]Bunz F, Hwang PM, Torrance C, Waldman T, Zhang Y, Dillehay L, et al. Disruption of p53 in human cancer cells alters the responses to therapeutic agents. J Clin Invest. 1999;104(3):263-9.
[31]Sobol RE, Guan Y-S, Li L-J, Zhang W-W, Peng Z, Menander KB, et al. Hainaut P, Oliver M, Wiman KG. Tp53 Gene Therapy for Cancer Treatment and Prevention. In: p53 in the Clinics. Heidelberg: Springer; 2013. Pp. 189-208.
[32]Roth JA. Adenovirus p53 gene therapy. Expert Opin Biol Ther. 2006;6(1):55-61.
[33]Tazawa H, Kagawa S, Fujiwara T. Advances in adenovirus-mediated p53 cancer gene therapy. Expert Opin Biol Ther. 2013;13(11):1569-83.
[34]Pearson S, Jia H, Kandachi K. China approves first gene therapy. Nat Biotechnol. 2004;22(1):3-4.
[35]Noori-Daloii MR, Maheronnaghsh R, Sayyah MK. Molecular genetics and gene therapy in esophageal cancer: A review article. Tehran Univ Med J. 2011;69(6):331-43. [Persian]
[36]Noori-Daloii MR, Tabarestani S. Molecular genetics, diagnosis and treatment of breast cancer: Review article. Sabzevar Univ Med Sci J. 2010;17(2):74-87. [Persian]
[37]Tassone P, Old M, Teknos TN, Pan Q. p53-based therapeutics for head and neck squamous cell carcinoma. Oral Oncol. 2013;49(8):733-7.
[38]Rogulski KR, Freytag SO, Zhang K, Gilbert JD, Paielli DL, Kim JH, et al. In vivo antitumor activity of ONYX-015 is influenced by p53 status and is augmented by radiotherapy. Cancer Res. 2000;60(5):1193-6.
[39]Zhang Y, Xiong Y. Control of p53 ubiquitination and nuclear export by MDM2 and ARF. Cell Growth Differ. 2001;12(4):175-86.
[40]de Rozieres S, Maya R, Oren M, Lozano G. The loss of mdm2 induces p53-mediated apoptosis. Oncogene. 2000;19(13):1691-7.
[41]Wang H, Nan L, Yu D, Lindsey JR, Agrawal S, Zhang R. Anti-tumor efficacy of a novel antisense anti-MDM2 mixed-backbone oligonucleotide in human colon cancer models: p53-dependent and p53-independent mechanisms. Mol Med. 2002;8(4):185-99.
[42]Kussie PH, Gorina S, Marechal V, Elenbaas B, Moreau J, Levine AJ, et al. Structure of the MDM2 oncoprotein bound to the p53 tumor suppressor transactivation domain. Science. 1996;274(5289):948-53.
[43]Bassett EA, Wang W, Rastinejad F, El-Deiry WS. Structural and functional basis for therapeutic modulation of p53 signaling. Clin Cancer Res. 2008;14(20):6376-86.
[44]Vassilev LT, Vu BT, Graves B, Carvajal D, Podlaski F, Filipovic Z, et al. In vivo activation of the p53 pathway by small-molecule antagonists of MDM2. Science. 2004;303(5659):844-8.
[45]Haaland I, Opsahl JA, Berven FS, Reikvam H, Fredly HK, Haugse R, et al. Molecular mechanisms of nutlin-3 involve acetylation of p53, histones and heat shock proteins in acute myeloid leukemia. Mol Cancer. 2014;13:116.
[46]Gu L, Zhu N, Findley HW, Zhou M. MDM2 antagonist nutlin-3 is a potent inducer of apoptosis in pediatric acute lymphoblastic leukemia cells with wild-type p53 and overexpression of MDM2. Leukemia. 2008;22(4):730-9.
[47]Supiot S, Hill RP, Bristow RG. Nutlin-3 radiosensitizes hypoxic prostate cancer cells independent of p53. Mol Cancer Ther. 2008;7(4):993-9.
[48]Koblish HK, Zhao S, Franks CF, Donatelli RR, Tominovich RM, LaFrance LV, et al. Benzodiazepinedione inhibitors of the Hdm2: p53 complex suppress human tumor cell proliferation in vitro and sensitize tumors to doxorubicin in vivo. Mol Cancer Ther. 2006;5(1):160-9.
[49]Shangary S, Ding K, Qiu S, Nikolovska-Coleska Z, Bauer JA, Liu M, et al. Reactivation of p53 by a specific MDM2 antagonist (MI-43) leads to p21-mediated cell cycle arrest and selective cell death in colon cancer. Mol Cancer Ther. 2008;7(6):1533-42.
[50]Ding K, Lu Y, Nikolovska-Coleska Z, Wang G, Qiu S, Shangary S, et al. Structure-based design of spiro-oxindoles as potent, specific small-molecule inhibitors of the MDM2-p53 interaction. J Med Chem. 2006;49(12):3432-5.
[51]Yang Y, Ludwig RL, Jensen JP, Pierre SA, Medaglia MV, Davydov IV, et al. Small molecule inhibitors of HDM2 ubiquitin ligase activity stabilize and activate p53 in cells. Cancer Cell. 2005;7(6):547-59.
[52]Nag S, Zhang X, Srivenugopal KS, Wang MH, Wang W, Zhang R. Targeting MDM2-p53 interaction for cancer therapy: are we there yet?. Curr Med Chem. 2014;21(5):553-74.
[53]Lau LM, Nugent JK, Zhao X, Irwin MS. HDM2 antagonist Nutlin-3 disrupts p73-HDM2 binding and enhances p73 function. Oncogene. 2008;27(7):997-1003.
[54]Gu L, Zhu N, Zhang H, Durden DL, Feng Y, Zhou M. Regulation of XIAP translation and induction by MDM2 following irradiation. Cancer Cell. 2009;15(5):363-75.
[55]Haigis MC, Guarente LP. Mammalian sirtuins-emerging roles in physiology, aging and calorie restriction. Genes Dev. 2006;20(21):2913-21.
[56]Luo J, Li M, Tang Y, Laszkowska M, Roeder RG, Gu W. Acetylation of p53 augments its site-specific DNA binding both in vitro and in vivo. Proc Natl Acad Sci U S A. 2004;101(8):2259-64.
[57]Sasca D, Hähnel PS, Szybinski J, Khawaja K, Kriege O, Pante SV, et al. SIRT1 prevents genotoxic stress-induced p53 activation in acute myeloid leukemia. Blood. 2014;124(1):121-33.
[58]Lain S, Hollick JJ, Campbell J, Staples OD, Higgins M, Aoubala M, et al. Discovery, in vivo activity, and mechanism of action of a small-molecule p53 activator. Cancer Cell. 2008;13(5):454-63.
[59]Gudkov AV, Komarova EA. Dangerous habits of a security guard: the two faces of p53 as a drug target. Hum Mol Genet. 2007;16 Spec No 1:R67-72.
[60]Strom E, Sathe S, Komarov PG, Chernova OB, Pavlovska I, Shyshynova I, et al. Small-molecule inhibitor of p53 binding to mitochondria protects mice from gamma radiation. Nat Chem Biol. 2006;2(9):474-9.
[61]Friedler A, Hansson LO, Veprintsev DB, Freund SM, Rippin TM, Nikolova PV, et al. A peptide that binds and stabilizes p53 core domain: chaperone strategy for rescue of oncogenic mutants. Proc Natl Acad Sci U S A. 2002;99(2):937-42.
[62]Issaeva N, Friedler A, Bozko P, Wiman KG, Fersht AR, Selivanova G. Rescue of mutants of the tumor suppressor p53 in cancer cells by a designed peptide. Proc Natl Acad Sci U S A. 2003;100(23):13303-7.
[63]Rippin TM, Bykov VJ, Freund SM, Selivanova G, Wiman KG, Fersht AR. Characterization of the p53-rescue drug CP-31398 in vitro and in living cells. Oncogene. 2002;21(14):2119-29.
[64]Tang X, Zhu Y, Han L, Kim AL, Kopelovich L, Bickers DR, et al. CP-31398 restores mutant p53 tumor suppressor function and inhibits UVB-induced skin carcinogenesis in mice. J Clin Invest. 2007;117(12):3753-64.
[65]Bykov VJ, Issaeva N, Zache N, Shilov A, Hultcrantz M, Bergman J, et al. Reactivation of mutant p53 and induction of apoptosis in human tumor cells by maleimide analogs. J Biol Chem. 2005;280(34):30384-91
[66]Bykov VJ, Wiman KG. Mutant p53 reactivation by small molecules makes its way to the clinic. FEBS Lett. 2014;588(16):2622-7.
[67]Lambert JM, Gorzov P, Veprintsev DB, Söderqvist M, Segerbäck D, Bergman J, et al. PRIMA-1 reactivates mutant p53 by covalent binding to the core domain. Cancer Cell. 2009;15(5):376-88.
[68]Li Y, Mao Y, Brandt-Rauf PW, Williams AC, Fine RL. Selective induction of apoptosis in mutant p53 premalignant and malignant cancer cells by PRIMA-1 through the c-Jun-NH2-kinase pathway. Mol Cancer Ther. 2005;4(6):901-9.
[69]Supiot S, Zhao H, Wiman K, Hill RP, Bristow RG. PRIMA-1(met) radiosensitizes prostate cancer cells independent of their MTp53-status. Radiother Oncol. 2008;86(3):407-11.
[70]Sugikawa E, Hosoi T, Yazaki N, Gamanuma M, Nakanishi N, Ohashi M. Mutant p53 mediated induction of cell cycle arrest and apoptosis at G1 phase by 9-hydroxyellipticine. Anticancer Res. 1999;19(4B):3099-108.
[71]Pamarthy D, Tan M, Wu M, Chen J, Yang D, Wang S, et al. p27 degradation by an ellipticinium series of compound via ubiquitin-proteasome pathway. Cancer Biol Ther. 2007;6(3):360-6.
[72]North S, Pluquet O, Maurici D, El-Ghissassi F, Hainaut P. Restoration of wild-type conformation and activity of a temperature-sensitive mutant of p53 (p53(V272M)) by the cytoprotective aminothiol WR1065 in the esophageal cancer cell line TE-1. Mol Carcinog. 2002;33(3):181-8.
[73]Weinmann L, Wischhusen J, Demma MJ, Naumann U, Roth P, Dasmahapatra B, et al. A novel p53 rescue compound induces p53-dependent growth arrest and sensitises glioma cells to Apo2L/TRAIL-induced apoptosis. Cell Death Differ. 2008;15(4):718-29.
[74]Kaelin WG Jr. The concept of synthetic lethality in the context of anticancer therapy. Nat Rev Cancer. 2005;5(9):689-98.
[75]Fang B. Development of synthetic lethality anticancer therapeutics. J Med Chem. 2014;57(19):7859-73.
[76]Zhang CC, Yang JM, Bash-Babula J, White E, Murphy M, Levine AJ, et al. DNA damage increases sensitivity to vinca alkaloids and decreases sensitivity to taxanes through p53-dependent repression of microtubule-associated protein 4. Cancer Res. 1999;59(15):3663-70.
[77]Buzzai M, Jones RG, Amaravadi RK, Lum JJ, DeBerardinis RJ, Zhao F, et al. Systemic treatment with the antidiabetic drug metformin selectively impairs p53-deficient tumor cell growth. Cancer Res. 2007;67(14):6745-52.
[78]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):956-65.
[79]Wang Y, Li J, Booher RN, Kraker A, Lawrence T, Leopold WR, et al. Radiosensitization of p53 mutant cells by PD0166285, a novel G(2) checkpoint abrogator. Cancer Res. 2001;61(22):8211-7.
[80]Lu J, Bai L, Sun H, Nikolovska-Coleska Z, McEachern D, Qiu S, et al. SM-164: A novel, bivalent Smac mimetic that induces apoptosis and tumor regression by concurrent removal of the blockade of cIAP-1/2 and XIAP. Cancer Res. 2008;68(22):9384-93.
[2]Noori-Daloii MR. Medical molecular genetics in the third millennium. Tehran: Nashr-e-akhar; 2009. [Persian]
[3]Turnpenny PD, Ellard S. Principles of medical genetics Emery’s elements of medical genetics. Noori Daloii MR (Translator). 14th ed. Tehran: Jame’e Negar; 2012. [Persian]
[4]Lane DP, Crawford LV. T antigen is bound to a host protein in SY40-transformed cells. Nature. 1979;278:261-3.
[5]Baker SJ, Fearon ER, Nigro JM, Hamilton SR, Preisinger AC, Jessup JM, et al. Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas. Science. 1989;244(4901):217-21.
[6]Finlay CA, Hinds PW, Levine AJ. The p53 proto-oncogene can act as a suppressor of transformation. Cell. 1989;57(7):1083-93.
[7]Vazquez A, Bond EE, Levine AJ, Bond GL. The genetics of the p53 pathway, apoptosis and cancer therapy. Nat Rev Drug Discov. 2008;7(12):979-87.
[8]Vogelstein B, Lane D, Levine AJ. Surfing the p53 network. Nature. 2000;408(6810):307-10.
[9]Dornan D, Wertz I, Shimizu H, Arnott D, Frantz GD, Dowd P, et al. The ubiquitin ligase COP1 is a critical negative regulator of p53. Nature. 2004;429(6987):86-92.
[10]Leng RP, Lin Y, Ma W, Wu H, Lemmers B, Chung S, et al. Pirh2, a p53-induced ubiquitin-protein ligase, promotes p53 degradation. Cell. 2003;112(6):779-91.
[11]Bullock AN, Henckel J, Fersht AR. Quantitative analysis of residual folding and DNA binding in mutant p53 core domain: Definition of mutant states for rescue in cancer therapy. Oncogene. 2000;19(10):1245-56.
[12]Noori-Daloii MR, Yaghoubi MM. Apoptosis or programmed cell death and cancer. Tehran: 6th Razi Conference of Medical Sciences; 2000. [Persian]
[13]Noori-Daloii MR, Vand Rajabpour F. Roles of miRNAs in gene expression regulation, apoptosis, diagnosis and treatment of cancer. Med Sci J Islamic Azad Univ Tehran Med Branch. 2011;21(3):151-161. [Persian]
[14]Tiwari M. Apoptosis, angiogenesis and cancer therapies. J Cancer Ther Res. 2012;1(1):3.
[15]Carmeliet P. Angiogenesis in health and disease. Nat Med. 2003;9(6):653-60.
[16]Sharma MR, Tuszynski GP, Sharma MC. Angiostatin-induced inhibition of endothelial cell proliferation/apoptosis is associated with the down-regulation of cell cycle regulatory protein cdk5. J Cell Biochem. 2004;91(2):398-409.
[17]Browder T, Folkman J, Pirie-Shepherd S. The hemostatic system as a regulator of angiogenesis. J Biol Chem. 2000;275(3):1521-4.
[18]Jiang L, Sheikh MS, Huang Y. Decision making by p53: Life versus death. Mol Cell Pharmacol. 2010;2(2):69-77.
[19]Sridhar SS, Shepherd FA. Targeting angiogenesis: A review of angiogenesis inhibitors in the treatment of lung cancer. Lung Cancer. 2003;42 Suppl 1:S81-91.
[20]Kelly PN, Strasser A. The role of Bcl-2 and its pro-survival relatives in tumourigenesis and cancer therapy. Cell Death Differ. 2011;18(9):1414-24.
[21]Kim K, Jeong KW, Kim H, Choi J, Lu W, Stallcup MR, et al. Functional interplay between p53 acetylation and H1. 2 phosphorylation in p53-regulated transcription. Oncogene. 2012;31(39):4290-301.
[22]Nicholls P, Mason MG, Cooper CE. Cytochrome c oxidase heme and Cu centres: Redox and spectral interactions. Biochimica et Biophysica Acta (BBA)-Bioenergetics. 2012;1817:S111.
[23]Manzl C, Fava L, Krumschnabel G, Peintner L, Tanzer M, Soratroi C, et al. Death of p53-defective cells triggered by forced mitotic entry in the presence of DNA damage is not uniquely dependent on Caspase-2 or the PIDDosome. Cell Death Disease. 2013;4(12):e942.
[24]Dorstyn L, Puccini J, Wilson C, Shalini S, Nicola M, Moore S, et al. Caspase-2 deficiency promotes aberrant DNA-damage response and genetic instability. Cell Death Differ. 2012;19(8):1288-98
[25]El-Deiry WS. The role of p53 in chemosensitivity and radiosensitivity. Oncogene. 2003;22(47):7486-95.
[26]Lowe SW, Bodis S, McClatchey A, Remington L, Ruley HE, Fisher DE, et al. p53 status and the efficacy of cancer therapy in vivo. Science. 1994;266(5186):807-10.
[27]Lu C, El-Deiry WS. Targeting p53 for enhanced radio- and chemo-sensitivity. Apoptosis. 2009;14(4):597-606.
[28]Williams JR, Zhang Y, Zhou H, Gridley DS, Koch CJ, Russell J, et al. A quantitative overview of radiosensitivity of human tumor cells across histological type and TP53 status. Int J Radiat Biol. 2008;84(4):253-64.
[29]Bertheau P, Plassa F, Espié M, Turpin E, de Roquancourt A, Marty M, et al. Effect of mutated TP53 on response of advanced breast cancers to high-dose chemotherapy. Lancet. 2002;360(9336):852-4.
[30]Bunz F, Hwang PM, Torrance C, Waldman T, Zhang Y, Dillehay L, et al. Disruption of p53 in human cancer cells alters the responses to therapeutic agents. J Clin Invest. 1999;104(3):263-9.
[31]Sobol RE, Guan Y-S, Li L-J, Zhang W-W, Peng Z, Menander KB, et al. Hainaut P, Oliver M, Wiman KG. Tp53 Gene Therapy for Cancer Treatment and Prevention. In: p53 in the Clinics. Heidelberg: Springer; 2013. Pp. 189-208.
[32]Roth JA. Adenovirus p53 gene therapy. Expert Opin Biol Ther. 2006;6(1):55-61.
[33]Tazawa H, Kagawa S, Fujiwara T. Advances in adenovirus-mediated p53 cancer gene therapy. Expert Opin Biol Ther. 2013;13(11):1569-83.
[34]Pearson S, Jia H, Kandachi K. China approves first gene therapy. Nat Biotechnol. 2004;22(1):3-4.
[35]Noori-Daloii MR, Maheronnaghsh R, Sayyah MK. Molecular genetics and gene therapy in esophageal cancer: A review article. Tehran Univ Med J. 2011;69(6):331-43. [Persian]
[36]Noori-Daloii MR, Tabarestani S. Molecular genetics, diagnosis and treatment of breast cancer: Review article. Sabzevar Univ Med Sci J. 2010;17(2):74-87. [Persian]
[37]Tassone P, Old M, Teknos TN, Pan Q. p53-based therapeutics for head and neck squamous cell carcinoma. Oral Oncol. 2013;49(8):733-7.
[38]Rogulski KR, Freytag SO, Zhang K, Gilbert JD, Paielli DL, Kim JH, et al. In vivo antitumor activity of ONYX-015 is influenced by p53 status and is augmented by radiotherapy. Cancer Res. 2000;60(5):1193-6.
[39]Zhang Y, Xiong Y. Control of p53 ubiquitination and nuclear export by MDM2 and ARF. Cell Growth Differ. 2001;12(4):175-86.
[40]de Rozieres S, Maya R, Oren M, Lozano G. The loss of mdm2 induces p53-mediated apoptosis. Oncogene. 2000;19(13):1691-7.
[41]Wang H, Nan L, Yu D, Lindsey JR, Agrawal S, Zhang R. Anti-tumor efficacy of a novel antisense anti-MDM2 mixed-backbone oligonucleotide in human colon cancer models: p53-dependent and p53-independent mechanisms. Mol Med. 2002;8(4):185-99.
[42]Kussie PH, Gorina S, Marechal V, Elenbaas B, Moreau J, Levine AJ, et al. Structure of the MDM2 oncoprotein bound to the p53 tumor suppressor transactivation domain. Science. 1996;274(5289):948-53.
[43]Bassett EA, Wang W, Rastinejad F, El-Deiry WS. Structural and functional basis for therapeutic modulation of p53 signaling. Clin Cancer Res. 2008;14(20):6376-86.
[44]Vassilev LT, Vu BT, Graves B, Carvajal D, Podlaski F, Filipovic Z, et al. In vivo activation of the p53 pathway by small-molecule antagonists of MDM2. Science. 2004;303(5659):844-8.
[45]Haaland I, Opsahl JA, Berven FS, Reikvam H, Fredly HK, Haugse R, et al. Molecular mechanisms of nutlin-3 involve acetylation of p53, histones and heat shock proteins in acute myeloid leukemia. Mol Cancer. 2014;13:116.
[46]Gu L, Zhu N, Findley HW, Zhou M. MDM2 antagonist nutlin-3 is a potent inducer of apoptosis in pediatric acute lymphoblastic leukemia cells with wild-type p53 and overexpression of MDM2. Leukemia. 2008;22(4):730-9.
[47]Supiot S, Hill RP, Bristow RG. Nutlin-3 radiosensitizes hypoxic prostate cancer cells independent of p53. Mol Cancer Ther. 2008;7(4):993-9.
[48]Koblish HK, Zhao S, Franks CF, Donatelli RR, Tominovich RM, LaFrance LV, et al. Benzodiazepinedione inhibitors of the Hdm2: p53 complex suppress human tumor cell proliferation in vitro and sensitize tumors to doxorubicin in vivo. Mol Cancer Ther. 2006;5(1):160-9.
[49]Shangary S, Ding K, Qiu S, Nikolovska-Coleska Z, Bauer JA, Liu M, et al. Reactivation of p53 by a specific MDM2 antagonist (MI-43) leads to p21-mediated cell cycle arrest and selective cell death in colon cancer. Mol Cancer Ther. 2008;7(6):1533-42.
[50]Ding K, Lu Y, Nikolovska-Coleska Z, Wang G, Qiu S, Shangary S, et al. Structure-based design of spiro-oxindoles as potent, specific small-molecule inhibitors of the MDM2-p53 interaction. J Med Chem. 2006;49(12):3432-5.
[51]Yang Y, Ludwig RL, Jensen JP, Pierre SA, Medaglia MV, Davydov IV, et al. Small molecule inhibitors of HDM2 ubiquitin ligase activity stabilize and activate p53 in cells. Cancer Cell. 2005;7(6):547-59.
[52]Nag S, Zhang X, Srivenugopal KS, Wang MH, Wang W, Zhang R. Targeting MDM2-p53 interaction for cancer therapy: are we there yet?. Curr Med Chem. 2014;21(5):553-74.
[53]Lau LM, Nugent JK, Zhao X, Irwin MS. HDM2 antagonist Nutlin-3 disrupts p73-HDM2 binding and enhances p73 function. Oncogene. 2008;27(7):997-1003.
[54]Gu L, Zhu N, Zhang H, Durden DL, Feng Y, Zhou M. Regulation of XIAP translation and induction by MDM2 following irradiation. Cancer Cell. 2009;15(5):363-75.
[55]Haigis MC, Guarente LP. Mammalian sirtuins-emerging roles in physiology, aging and calorie restriction. Genes Dev. 2006;20(21):2913-21.
[56]Luo J, Li M, Tang Y, Laszkowska M, Roeder RG, Gu W. Acetylation of p53 augments its site-specific DNA binding both in vitro and in vivo. Proc Natl Acad Sci U S A. 2004;101(8):2259-64.
[57]Sasca D, Hähnel PS, Szybinski J, Khawaja K, Kriege O, Pante SV, et al. SIRT1 prevents genotoxic stress-induced p53 activation in acute myeloid leukemia. Blood. 2014;124(1):121-33.
[58]Lain S, Hollick JJ, Campbell J, Staples OD, Higgins M, Aoubala M, et al. Discovery, in vivo activity, and mechanism of action of a small-molecule p53 activator. Cancer Cell. 2008;13(5):454-63.
[59]Gudkov AV, Komarova EA. Dangerous habits of a security guard: the two faces of p53 as a drug target. Hum Mol Genet. 2007;16 Spec No 1:R67-72.
[60]Strom E, Sathe S, Komarov PG, Chernova OB, Pavlovska I, Shyshynova I, et al. Small-molecule inhibitor of p53 binding to mitochondria protects mice from gamma radiation. Nat Chem Biol. 2006;2(9):474-9.
[61]Friedler A, Hansson LO, Veprintsev DB, Freund SM, Rippin TM, Nikolova PV, et al. A peptide that binds and stabilizes p53 core domain: chaperone strategy for rescue of oncogenic mutants. Proc Natl Acad Sci U S A. 2002;99(2):937-42.
[62]Issaeva N, Friedler A, Bozko P, Wiman KG, Fersht AR, Selivanova G. Rescue of mutants of the tumor suppressor p53 in cancer cells by a designed peptide. Proc Natl Acad Sci U S A. 2003;100(23):13303-7.
[63]Rippin TM, Bykov VJ, Freund SM, Selivanova G, Wiman KG, Fersht AR. Characterization of the p53-rescue drug CP-31398 in vitro and in living cells. Oncogene. 2002;21(14):2119-29.
[64]Tang X, Zhu Y, Han L, Kim AL, Kopelovich L, Bickers DR, et al. CP-31398 restores mutant p53 tumor suppressor function and inhibits UVB-induced skin carcinogenesis in mice. J Clin Invest. 2007;117(12):3753-64.
[65]Bykov VJ, Issaeva N, Zache N, Shilov A, Hultcrantz M, Bergman J, et al. Reactivation of mutant p53 and induction of apoptosis in human tumor cells by maleimide analogs. J Biol Chem. 2005;280(34):30384-91
[66]Bykov VJ, Wiman KG. Mutant p53 reactivation by small molecules makes its way to the clinic. FEBS Lett. 2014;588(16):2622-7.
[67]Lambert JM, Gorzov P, Veprintsev DB, Söderqvist M, Segerbäck D, Bergman J, et al. PRIMA-1 reactivates mutant p53 by covalent binding to the core domain. Cancer Cell. 2009;15(5):376-88.
[68]Li Y, Mao Y, Brandt-Rauf PW, Williams AC, Fine RL. Selective induction of apoptosis in mutant p53 premalignant and malignant cancer cells by PRIMA-1 through the c-Jun-NH2-kinase pathway. Mol Cancer Ther. 2005;4(6):901-9.
[69]Supiot S, Zhao H, Wiman K, Hill RP, Bristow RG. PRIMA-1(met) radiosensitizes prostate cancer cells independent of their MTp53-status. Radiother Oncol. 2008;86(3):407-11.
[70]Sugikawa E, Hosoi T, Yazaki N, Gamanuma M, Nakanishi N, Ohashi M. Mutant p53 mediated induction of cell cycle arrest and apoptosis at G1 phase by 9-hydroxyellipticine. Anticancer Res. 1999;19(4B):3099-108.
[71]Pamarthy D, Tan M, Wu M, Chen J, Yang D, Wang S, et al. p27 degradation by an ellipticinium series of compound via ubiquitin-proteasome pathway. Cancer Biol Ther. 2007;6(3):360-6.
[72]North S, Pluquet O, Maurici D, El-Ghissassi F, Hainaut P. Restoration of wild-type conformation and activity of a temperature-sensitive mutant of p53 (p53(V272M)) by the cytoprotective aminothiol WR1065 in the esophageal cancer cell line TE-1. Mol Carcinog. 2002;33(3):181-8.
[73]Weinmann L, Wischhusen J, Demma MJ, Naumann U, Roth P, Dasmahapatra B, et al. A novel p53 rescue compound induces p53-dependent growth arrest and sensitises glioma cells to Apo2L/TRAIL-induced apoptosis. Cell Death Differ. 2008;15(4):718-29.
[74]Kaelin WG Jr. The concept of synthetic lethality in the context of anticancer therapy. Nat Rev Cancer. 2005;5(9):689-98.
[75]Fang B. Development of synthetic lethality anticancer therapeutics. J Med Chem. 2014;57(19):7859-73.
[76]Zhang CC, Yang JM, Bash-Babula J, White E, Murphy M, Levine AJ, et al. DNA damage increases sensitivity to vinca alkaloids and decreases sensitivity to taxanes through p53-dependent repression of microtubule-associated protein 4. Cancer Res. 1999;59(15):3663-70.
[77]Buzzai M, Jones RG, Amaravadi RK, Lum JJ, DeBerardinis RJ, Zhao F, et al. Systemic treatment with the antidiabetic drug metformin selectively impairs p53-deficient tumor cell growth. Cancer Res. 2007;67(14):6745-52.
[78]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):956-65.
[79]Wang Y, Li J, Booher RN, Kraker A, Lawrence T, Leopold WR, et al. Radiosensitization of p53 mutant cells by PD0166285, a novel G(2) checkpoint abrogator. Cancer Res. 2001;61(22):8211-7.
[80]Lu J, Bai L, Sun H, Nikolovska-Coleska Z, McEachern D, Qiu S, et al. SM-164: A novel, bivalent Smac mimetic that induces apoptosis and tumor regression by concurrent removal of the blockade of cIAP-1/2 and XIAP. Cancer Res. 2008;68(22):9384-93.