| [1] Wei JX, Zaika E, Zaika A. p53 Family: Role of protein isoforms in Human Cancer. J Nucleic Acids, 2012, 2012: 687359.[2] Fernandez-Medarde A, Santos E. Ras in cancer and developmental diseases. Genes Cancer, 2011, 2(3): 344-358.[3] Hanahan D, Weinberg RA. The hallmarks of cancer. Cell, 2000, 100(1): 57-70.[4] Bálint É, Vousden KH. Activation and activities of the p53 tumour suppressor protein. Br J Cancer, 2001, 85(12): 1813-1823.[5] Livesey KM, Kang R, Vernon P, Buchser W, Loughran P, Watkins SC, Zhang L, Manfredi JJ, Zeh HJ 3rd, Li L, Lotze MT, Tang D. p53/HMGB1 complexes regulate autophagy and apoptosis. Cancer Res, 2012, 72(8): 1996-2005.[6] Dong XX, Wang YR, Qin S, Liang ZQ, Liu BH, Qin ZH, Wang Y. p53 Mediates autophagy activation and mitochondria dysfunction in kainic acid-induced excitotoxicity in primary striatal neurons. Neuroscience, 2012, 207: 52-64.[7] Shen L, Sun X, Fu ZH, Yang GD, Li JY, Yao LB. The fundamental role of the p53 pathway in tumor metabolism and its implication in tumor therapy. Clin Cancer Res, 2012, 18(6): 1561-1567.[8] Solomon H, Madar S, Rotter V. Mutant p53 gain of function is interwoven into the hallmarks of cancer. J Pathol, 2011, 225(4): 475-478.[9] Acin S, Li ZY, Mejia O, Roop DR, El-Naggar AK, Caulin C. Gain-of-function mutant p53 but not p53 deletion promotes head and neck cancer progression in response to oncogenic K-ras. J Pathol, 2011, 225(4): 479-489.[10] Kogan-Sakin I, Tabach Y, Buganim Y, Molchadsky A, Solomon H, Madar S, Kamer I, Stambolsky P, Shelly A, Goldfinger N, Valsesia-Wittmann S, Puisieux A, Zundelevich A, Gal-Yam EN, Avivi C, Barshack I, Brait M, Sidransky D, Domany E, Rotter V. Mutant p53R175H upregulates Twist1 expression and promotes epithelial-mesenchymal transition in immortalized prostate cells. Cell Death Differ, 2011, 18(2): 271-281.[11] Wang SP, Wang WL, Chang YL, Wu CT, Chao YC, Kao SH, Yuan A, Lin CW, Yang SC, Chan WK, Li KC, Hong TM, Yang PC. p53 controls cancer cell invasion by inducing the MDM2-mediated degradation of Slug. Nat Cell Biol, 2009, 11(6): 694-704.[12] Dhar G, Banerjee S, Dhar K, Tawfik O, Mayo MS, Vanveldhuizen PJ, Banerjee SK. Gain of oncogenic function of p53 mutants induces invasive phenotypes in human breast cancer cells by silencing CCN5/WISP-2. Cancer Res, 2008, 68(12): 4580-4587.[13] 李大虎, 张令强, 贺福初. 突变体p53研究进展. 遗传, 2008, 30(6): 697-703.[14] Lock R, Debnath J. Ras, autophagy and glycolysis. Cell Cycle, 2011, 10(10): 1516-1517.[15] Chesney J, Telang S. Regulation of glycolytic and mitochondrial metabolism by Ras. Curr Pharm Biotechnol, 2012, in press.[16] Downward J. Targeting RAS signalling pathways in cancer therapy. Nat Rev Cancer, 2003, 3(1): 11-22.[17] Cox AD, Der CJ. Ras family signaling: therapeutic targeting. Cancer Biol Ther, 2002, 1(6): 599-606.[18] Parada LF, Land H, Weinberg RA, Wolf D, Rotter V. Cooperation between gene encoding p53 tumour antigen and ras in cellular transformation. Nature, 1984, 312(5995): 649-651.[19] Eliyahu D, Raz A, Gruss P, Givol D, Oren M. Participation of p53 cellular tumour antigen in transformation of normal embryonic cells. Nature, 1984, 312(5995): 646-649.[20] Jia S, Zhao L, Tang W, Luo Y. The gain of function of p53 mutant p53S in promoting tumorigenesis by cross-talking with H-RasV12. Int J Biol Sci, 2012, 8(5): 596-605.[21] Buganim Y, Solomon H, Rais Y, Kistner D, Nachmany I, Brait M, Madar S, Goldstein I, Kalo E, Adam N, Gordin M, Rivlin N, Kogan I, Brosh R, Sefadia-Elad G, Goldfinger N, Sidransky D, Kloog Y, Rotter V. p53 Regulates the Ras circuit to inhibit the expression of a cancer-related gene signature by various molecular pathways. Cancer Res, 2010, 70(6): 2274-2284.[22] Boiko AD, Porteous S, Razorenova OV, Krivokrysenko VI, Williams BR, Gudkov AV. A systematic search for downstream mediators of tumor suppressor function of p53 reveals a major role of BTG2 in suppression of Ras- induced transformation. Genes Dev, 2006, 20(2): 236-252.[23] Buganim Y, Kalo E, Brosh R, Besserglick H, Nachmany I, Rais Y, Stambolsky P, Tang X, Milyavsky M, Shats I, Kalis M, Goldfinger N, Rotter V. Mutant p53 protects cells from 12-O-tetradecanoylphorbol-13-acetate-induced death by attenuating activating transcription factor 3 induction. Cancer Res, 2006, 66(22): 10750-10759.[24] DeNardo DG, Andreu P, Coussens LM. Interactions between lymphocytes and myeloid cells regulate pro-versus anti-tumor immunity. Cancer Metastasis Rev, 2010, 29(2): 309-316.[25] Qian BZ, Pollard JW. Macrophage diversity enhances tumor progression and metastasis. Cell, 2010, 141(1): 39-51.[26] Schetter AJ, Heegaard NHH, Harris CC. Inflammation and cancer: interweaving microRNA, free radical, cytokine and p53 pathways. Carcinogenesis, 2010, 31(1): 37-49.[27] Starczynowski DT, Lockwood WW, Delehouzee S, Chari R, Wegrzyn J, Fuller M, Tsao MS, Lam S, Gazdar AF, Lam WL, Karsan A. TRAF6 is an amplified oncogene bridging the RAS and NF-κB pathways in human lung cancer. J Clin Invest, 2011, 121(10): 4095-4105.[28] Min J, Zaslavsky A, Fedele G, McLaughlin SK, Reczek EE, De Raedt T, Guney I, Strochlic DE, Macconaill LE, Beroukhim R, Bronson RT, Ryeom S, Hahn WC, Loda M, Cichowski K. An oncogene-tumor suppressor cascade drives metastatic prostate cancer by coordinately activating Ras and nuclear factor-κB. Nat Med, 2010, 16(3): 286-294.[29] Tang XH, Milyavsky M, Shats I, Erez N, Goldfinger N, Rotter V. Activated p53 suppresses the histone methyltransferase EZH2 gene. Oncogene, 2004, 23(34): 5759-5769.[30] Meylan E, Dooley AL, Feldser DM, Shen L, Turk E, Ouyang C, Jacks T. Requirement for NF-κB signalling in a mouse model of lung adenocarcinoma. Nature, 2009, 462(7269): 104-107.[31] Kim HR, Roe JS, Lee JE, Hwang IY, Cho EJ, Youn HD. A p53-inducible microRNA-34a downregulates Ras signaling by targeting IMPDH. Biochem Biophys Res Commun, 2012, 418(4): 682-688.[32] He L, He X, Lim LP, de Stanchina E, Xuan Z, Liang Y, Xue W, Zender L, Magnus J, Ridzon D, Jackson AL, Linsley PS, Chen C, Lowe SW, Cleary MA, Hannon GJ. A microRNA component of the p53 tumour suppressor network. Nature, 2007, 447(7148): 1130-1134.[33] Tolbert D, Lu X, Yin C, Tantama M, Van Dyke T. p19ARF is dispensable for oncogenic stress-induced p53-mediated apoptosis and tumor suppression in vivo. Mol Cell Biol, 2002, 22(1): 370-377.[34] Yaswen P, Campisi J. Oncogene-induced senescence pathways weave an intricate tapestry. Cell, 2007, 128(2): 233-234.[35] Serrano M, Lin AW, McCurrach ME, Beach D, Lowe SW. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell, 1997, 88(5): 593-602.[36] Sreeramaneni R, Chaudhry A, McMahon M, Sherr CJ, Inoue K. Ras-Raf-Arf signaling critically depends on the Dmp1 transcription factor. Mol Cell Biol, 2004, 25(1): 220-232.[37] Inoue K, Wen R, Rehg JE, Adachi M, Cleveland JL, Roussel MF, Sherr CJ. Disruption of the ARF transcriptional activator DMP1 facilitates cell immortalization, Ras transformation, and tumorigenesis. Genes Dev, 2000, 14(14): 1797-1809.[38] McMahon M, Woods D. Regulation of the p53 pathway by Ras, the plot thickens. Biochim Biophys Acta, 2001, 1471(2): 63-71.[39] Sun PQ, Yoshizuka N, New L, Moser BA, Li YL, Liao R, Xie CC, Chen JM, Deng QD, Yamout M, Dong MQ, Frangou CG, Yates JR III, Wright PE, Han JH. PRAK is essential for ras-induced senescence and tumor suppression. Cell, 2007, 128(2): 295-308.[40] Ventura A, Kirsch DG, McLaughlin ME, Tuveson DA, Grimm J, Lintault L, Newman J, Reczek EE, Weissleder R, Jacks T. Restoration of p53 function leads to tumour regression in vivo. Nature, 2007, 445(7128): 661-665.[41] Xue W, Zender L, Miething C, Dickins RA, Hernando E, Krizhanovsky V, Cordon-Cardo C, Lowe SW. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature, 2007, 445(7128): 656-660.[42] Konishi H, Karakas B, Abukhdeir AM, Lauring J, Gustin JP, Garay JP, Konishi Y, Gallmeier E, Bachman KE, Park BH. Knock-in of mutant K-ras in nontumorigenic human epithelial cells as a new model for studying K-ras mediated transformation. Cancer Res, 2007, 67(18): 8460-8467.[43] Weinberg RA. Cancer biology and therapy: the road ahead. Cancer Biol Ther, 2002, 1(1): 3.[44] Tuveson DA, Shaw AT, Willis NA, Silver DP, Jackson EL, Chang S, Mercer KL, Grochow R, Hock H, Crowley D, Hingorani SR, Zaks T, King C, Jacobetz MA, Wang L, Bronson RT, Orkin SH, DePinho RA, Jacks T. Endogenous oncogenic K-rasG12D stimulates proliferation and widespread neoplastic and developmental defects. Cancer Cell, 2004, 5(4): 375-387.[45] Lee SH, Lee SJ, Jung YS, Xu YB, Kang HS, Ha NC, Park BJ. Blocking of p53-Snail binding, promoted by oncogenic K-Ras, recovers p53 expression and function. Neoplasia, 2009, 11(1): 22-31.[46] Halaschek-Wiener J, Wacheck V, Kloog Y, Jansen B. Ras inhibition leads to transcriptional activation of p53 and down-regulation of Mdm2: two mechanisms that cooperatively increase p53 function in colon cancer cells. Cell Signal, 2004, 16(11): 1319-1327.[47] Argast GM, Krueger JS, Thomson S, Sujka-Kwok I, Carey K, Silva S, O'Connor M, Mercado P, Mulford IJ, Young GD, Sennello R, Wild R, Pachter JA, Kan JL, Haley J, Rosenfeld-Franklin M, Epstein DM. Inducible expression of TGFβ, snail and Zeb1 recapitulates EMT in vitro and in vivo in a NSCLC model. Clin Exp Metas, 2011, 28(7): 593-614.[48] Haslehurst AM, Koti M, Dharsee M, Nuin P, Evans K, Geraci J, Childs T, Chen J, Li J, Weberpals J, Davey S, Squire J, Park PC, Feilotter H. EMT transcription factors snail and slug directly contribute to cisplatin resistance in ovarian cancer. BMC Cancer, 2012, 12(1): 91.[49] Kajita M, McClinic KN, Wade PA. Aberrant expression of the transcription factors snail and slug alters the response to genotoxic stress. Mol Cell Biol, 2004, 24(17): 7559-7566.[50] Lee SH, Park BJ. p53 activation by blocking snail: a novel pharmacological strategy for cancer. Curr Pharm Des, 2011, 17(6): 610-617.[51] Lee SH, Lee SJ, Chung JY, Jung YS, Choi SY, Hwang SH, Choi D, Ha NC, Park BJ. p53, secreted by K-Ras-Snail pathway, is endocytosed by K-Ras-mutated cells; implication of target-specific drug delivery and early diagnostic marker. Oncogene, 2009, 28(19): 2005-2014.[52] Shields JM, Pruitt K, McFall A, Shaub A, Der Channing J. Understanding ras: 'it ain't over 'til it's over'. Trends Cell Biol, 2000, 10(4): 147-154.[53] Braig M, Lee S, Loddenkemper C, Rudolph C, Peters AHFM, Schlegelberger B, Stein H, Dörken B, Jenuwein T, Schmitt CA. Oncogene-induced senescence as an initial barrier in lymphoma development. Nature, 2005, 436(7051): 660-665.[54] Xia M X, Land H. Tumor suppressor p53 restricts Ras stimulation of RhoA and cancer cell motility. Nat Struct Mol Biol, 2007, 14(3): 215-223.[55] Bos JL, Rehmann H, Wittinghofer A. GEFs and GAPs: critical elements in the control of small G proteins. Cell, 2007, 129(5): 865-877.[56] Rak J, Milsom C, Yu J. Tissue factor in cancer. Curr Opin Hematol, 2008, 15(5): 522-528.[57] Buller HR, van Doormaal FF, van Sluis GL, Kamphuisen PW. Cancer and thrombosis: from molecular mechanisms to clinical presentations. J Thromb Haemost: JTH, 2007, 5(Suppl. 1): 246-254.[58] Belting M, Dorrell MI, Sandgren S, Aguilar E, Ahamed J, Dorfleutner A, Carmeliet P, Mueller BM, Friedlander M, Ruf W. Regulation of angiogenesis by tissue factor cytoplasmic domain signaling. Nat Med, 2004, 10(5): 502-509.[59] Rickles FR, Shoji M, Abe K. The role of the hemostatic system in tumor growth, metastasis, and angiogenesis: tissue factor is a bifunctional molecule capable of inducing both fibrin deposition and angiogenesis in cancer. Int J Hemat, 2001, 73(2): 145-150.[60] Nakasaki T, Wada H, Shigemori C, Miki C, Gabazza EC, Nobori T, Nakamura S, Shiku H. Expression of tissue factor and vascular endothelial growth factor is associated with angiogenesis in colorectal cancer. Am J Hema-tol, 2002, 69(4): 247-254.[61] Yu JL, May L, Lhotak V, Shahrzad S, Shirasawa S, Weitz JI, Coomber BL, Mackman N, Rak JW. Oncogenic events regulate tissue factor expression in colorectal cancer cells: implications for tumor progression and angiogenesis. Blood, 2005, 105(4): 1734-1741.[62] Bunz F, Dutriaux A, Lengauer C, Waldman T, Zhou S, Brown JP, Sedivy JM, Kinzler KW, Vogelstein B. Requirement for p53 and p21 to sustain G2 arrest after DNA damage. Science, 1998, 282(5393): 1497-1501.[63] Levine AJ, Oren M. The first 30 years of p53: growing ever more complex. Nat Rev Cancer, 2009, 9(10): 749-758.[64] 陆思千, 贾舒婷, 罗瑛. 突变p53功能研究新进展与个性化的肿瘤治疗新策略. 遗传, 2011, 33(6): 539-548. |
