Combination therapy with p53–MDM2 binding inhibitors for malignancies
详细信息 查看全文
- 作者：Zegao Jin ; Jianfeng Shen ; Jingyao He ; Chunqi Hu
- 关键词：Nutlin ; 3 ; MIs ; p53–MDM2 binding inhibitors ; Anti ; cancer ; Combination therapy
- 刊名：Medicinal Chemistry Research
- 出版年：2015
- 出版时间：April 2015
- 年：2015
- 卷：24
- 期：4
- 页码：1369-1379
- 全文大小：657 KB
- 参考文献：1. Albihn, A, Mo, H, Yang, Y, Henriksson, M (2007) Camptothecin-induced apoptosis is enhanced by Myc and involves PKCdelta signaling. Int J Cancer 121: pp. 1821-1829 CrossRef
2. Azmi, AS, Aboukameel, A, Banerjee, S, Wang, Z, Mohammad, M, Wu, J, Wang, S, Yang, D, Philip, PA, Sarkar, FH, Mohammad, RM (2010) MDM2 inhibitor MI-319 in combination with cisplatin is an effective treatment for pancreatic cancer independent of p53 function. Eur J Cancer 46: pp. 1122-1131 CrossRef
3. Azmi, AS, Banerjee, S, Ali, S, Wang, Z, Bao, B, Beck, FW, Maitah, M, Choi, M, Shields, TF, Philip, PA, Sarkar, FH, Mohammad, RM (2011) Network modeling of MDM2 inhibitor-oxaliplatin combination reveals biological synergy in wt-p53 solid tumors. Oncotarget 2: pp. 378-392
4. Azmi, AS, Philip, PA, Aboukameel, A, Wang, Z, Banerjee, S, Zafar, SF, Goustin, AS, Almhanna, K, Yang, D, Sarkar, FH, Mohammad, RM (2010) Reactivation of p53 by novel MDM2 inhibitors: implications for pancreatic cancer therapy. Curr Cancer Drug Targets 10: pp. 319-331 CrossRef
5. Azmi, AS, Wang, ZW, Philip, PA, Mohammad, RM, Sarkar, FH (2010) Proof of concept: network and systems biology approaches aid in the discovery of potent anticancer drug combinations. Mol Cancer Ther 9: pp. 3137-3144 CrossRef
6. B?ttger, A, B?ttger, V, Sparks, A, Liu, W-L, Howard, SF, Lane, DP (1997) Design of a synthetic Mdm2-binding mini protein that activates the p53 response in vivo. Curr Biol 7: pp. 860-869 CrossRef
7. Binder, BR (2007) A novel application for murine double minute 2 antagonists: the p53 tumor suppressor network also controls angiogenesis. Circ Res 100: pp. 13-14 CrossRef
8. Blagosklonny, MV (2002) Sequential activation and inactivation of G2 checkpoints for selective killing of p53-deficient cells by microtubule-active drugs. Oncogene 21: pp. 6249-6254 CrossRef
9. Blagosklonny, MV, Robey, R, Bates, S, Fojo, T (2000) Pretreatment with DNA-damaging agents permits selective killing of checkpoint-deficient cells by microtubule-active drugs. J Clin Investig 105: pp. 533-539 CrossRef
10. Blandino, G, Levine, AJ, Oren, M (1999) Mutant p53 gain of function: differential effects of different p53 mutants on resistance of cultured cells to chemotherapy. Oncogene 18: pp. 477-485 CrossRef
11. Blaydes, JP, Gire, V, Rowson, JM, Wynford-Thomasa, D (1997) Tolerance of high levels of wild-type p53 in transformed epithelial cells dependent on auto-regulation by mdm-2. Oncogene 14: pp. 1859-1868 CrossRef
12. Bold, R (2004) Development of the proteasome inhibitor Velcade (TM) (Bortezomib) by Julian Adams, Ph.D., and Michael Kauffman, MD, Ph.D.. Cancer Investig 22: pp. 328-329 CrossRef
13. Canner, JA, Sobo, M, Ball, S, Hutzen, B, DeAngelis, S, Willis, W, Studebaker, AW, Ding, K, Wang, S, Yang, D, Lin, J (2009) MI-63: a novel small-molecule inhibitor targets MDM2 and induces apoptosis in embryonal and alveolar rhabdomyosarcoma cells with wild-type p53. Br J Cancer 101: pp. 774-781 CrossRef
14. Carvajal, D, Tovar, C, Yang, H, Vu, BT, Heimbrook, DC, Vassilev, LT (2005) Activation of p53 by MDM2 antagonists can protect proliferating cells from mitotic inhibitors. Cancer Res 65: pp. 1918-1924 CrossRef
15. Cheok, CF, Dey, A, Lane, DP (2007) Cyclin-dependent kinase inhibitors sensitize tumor cells to nutlin-induced apoptosis: a potent drug combination. Mol Cancer Res 5: pp. 1133-1145- 刊物主题：Pharmacology/Toxicology; Biochemistry, general; Cell Biology;
- 出版者：Springer US
- ISSN：1554-8120
文摘
p53 is a powerful tumor suppressor, and p53-a href='/search?dc.title=MDM2&facet-content-type=ReferenceWorkEntry&sortOrder=relevance' class='reference-link webtrekk-track' gaCategory="Internal link" gaLabel="MDM2" gaAction="reference keyword">MDM2 protein–protein interaction has been considered as an attractive cancer therapeutic target. More recently developed small molecules exert their effects by interrupting the p53-a href='/search?dc.title=MDM2&facet-content-type=ReferenceWorkEntry&sortOrder=relevance' class='reference-link webtrekk-track' gaCategory="Internal link" gaLabel="MDM2" gaAction="reference keyword">MDM2 binding and enhancing the anti-proliferative activities of p53. Small molecules such as Nutlin, MI-63, MI-219, and MI-319 that can activate p53 have shown their anti-tumor effects in different types of malignancies. Drug combinations between p53-a href='/search?dc.title=MDM2&facet-content-type=ReferenceWorkEntry&sortOrder=relevance' class='reference-link webtrekk-track' gaCategory="Internal link" gaLabel="MDM2" gaAction="reference keyword">MDM2 binding inhibitors with the other anti-proliferative small molecules may allow reduction in the amount of single component with a lower incidence of side effects or better therapeutic effects. In this current review, we present the recent achievements in combination applications between p53-a href='/search?dc.title=MDM2&facet-content-type=ReferenceWorkEntry&sortOrder=relevance' class='reference-link webtrekk-track' gaCategory="Internal link" gaLabel="MDM2" gaAction="reference keyword">MDM2 binding inhibitors with other small molecules in malignancies. In addition, we discuss how this combination holds promise as a therapeutic strategy for recent and future novel therapies in these diseases.