Inhibiting the interaction of cMET and IGF-1R with FAK effectively reduces growth of pancreatic cancer cells in vitro and in vivo

Anti-Cancer Agents in Medicinal Chemistry

Volumn 13, Issue 4, 2013, Pages 595-602

  Ucar, Deniz A ^a   Magis, Andrew T ^b   He, Di Hua ^a   Lawrence, Nicholas J ^c   Sebti, Said M ^c   Kurenova, Elena ^d   Zajac Kaye, Maria ^a   Zhang, Jianliang ^d   Hochwald, Steven N ^d  

^a UNIVERSITY OF FLORIDA COLLEGE OF MEDICINE   (United States)

^b UNIVERSITY OF ILLINOIS AT URBANA CHAMPAIGN   (United States)

^c H LEE MOFFITT CANCER CENTER AND RESEARCH INSTITUTE   (United States)

^d ROSWELL PARK CANCER INSTITUTE   (United States)

Author keywords

FAK; IGF 1R; Pancreatic cancer; Protein interactions

Indexed keywords

FOCAL ADHESION KINASE; FOCAL ADHESION KINASE INHIBITOR; GEMCITABINE; INT 231; PROTEIN KINASE B; SCATTER FACTOR RECEPTOR; SOMATOMEDIN C RECEPTOR; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CANCER INHIBITION; CELL VIABILITY; CHEMOSENSITIVITY; CONTROLLED STUDY; DRUG STRUCTURE; ENZYME ACTIVITY; HUMAN; HUMAN CELL; HUMAN TISSUE; IMMUNOBLOTTING; MOUSE; NONHUMAN; PANCREAS CANCER; PROTEIN INTERACTION; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; TUMOR GROWTH;

ANIMALS; ANTINEOPLASTIC AGENTS; CELL PROLIFERATION; CELL SURVIVAL; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG SCREENING ASSAYS, ANTITUMOR; FOCAL ADHESION PROTEIN-TYROSINE KINASES; HUMANS; MICE; MICE, NUDE; MOLECULAR STRUCTURE; PANCREATIC NEOPLASMS; PHOSPHORYLATION; PROTEIN BINDING; PROTEIN KINASE INHIBITORS; PROTO-ONCOGENE PROTEINS C-MET; PURINE NUCLEOSIDES; RECEPTOR, IGF TYPE 1; SIGNAL TRANSDUCTION; STRUCTURE-ACTIVITY RELATIONSHIP; TUMOR CELLS, CULTURED;

EID: 84876742817     PISSN: 18715206     EISSN: 18755992     Source Type: Journal    
DOI: 10.2174/1871520611313040009     Document Type: Article

References (31)

1. Yang, GY.; Wagner, T.D.; Fuss, M.; Thomas, CR Jr. Multimodality approaches for pancreatic cancer. C.A. Cancer J. Clin., 2005, 55(6), 352-367.
2. Kircher, SM.; Krantz, SB.; Nimeiri, HS.; Mulcahy, MF.; Munshi, HG.; Benson AB 3rd. Therapy of locally advanced pancreatic adenocarcinoma: unresectable and borderline patients. Expert Rev. Anticancer Ther., 2011, 11(10),1555-1565.
3. Philip P.A, Mooney, M, Jaffe, D, Eckhardt, G, Moore, M, Meropol, N, Emens, L, O'Reilly, E, Korc, M, Ellis, L, Benedetti, J, Rothenberg, M, Willett, C, Tempero, M, Lowy, A, Abbruzzese, J, Simeone, D, Hingorani, S, Berlin, J, Tepper, J. Consensus report of the national cancer institute clinical trials planning meeting on pancreas cancer treatment. J. Clin. Oncol., 2009, 27(33), 5660-5669.
4. Preis M, Korc M. Signaling pathways in pancreatic cancer. Crit. Rev. Eukaryot. Gene Expr., 2011, 21(2), 115-129.
5. Peters, S.; Adjei, AA. MET: a promising anticancer therapeutic target. Nat. Rev. Clin. Oncol., 2012, 9 (6), 314-326.
6. Li, C.; Wu, JJ.; Hynes, M.; Dosch, J.; Sarkar, B.; Welling, TH.; Pasca di Magliano, M.; Simeone, DM. c-Met is a marker of pancreatic cancer stem cells and therapeutic target. Gastroenterolog,. 2011, 141(6), 2218-2227.
7. Shah, AN.; Summy, JM.; Zhang, J.; Park, SI.; Parikh, NU.; Gallick, GE. Development and characterization of gemcitabine-resistant pancreatic tumor cells. Ann. Surg. Oncol., 2007, 14 (12), 3629-3637.
8. Chen, SY.; Chen, HC: Direct interaction of focal adhesion kinase (FAK) with Met is required for FAK to promote hepatocyte growth factor-induced cell invasion. Mol. Cell Biol., 2006, 26, 5155-5167.
9. Pollak, M. Insulin and insulin-like growth factor signalling in neoplasia. Nat. Rev. Cancer, 2008, 8(12), 915-928.
10. Ioannou N.; Seddon, AM.; Dalgleish, A.; Mackintosh, D.; Modjtahedi, H. Expression pattern and targeting of HER family members and IGF-IR in pancreatic cancer. Front Biosci., 2012, 17, 2698-724.
11. Liu, W.; Bloom, D.A.; Cance, W.G.; Kurenova, E.V.; Golubovskaya, V.M.; and Hochwald, S.N. FAK and IGF-IR interact to provide survival signals in human pancreatic adenocarcinoma cells. Carcinogenesis, 2008, 29(6), 1096-1107.
12. Zheng, D.; Golubovskaya, V.; Kurenova, E.; Wood, C.; Massoll, N.A.; Ostrov, D.; Cance, W.G.; and Hochwald, S.N. A novel strategy to inhibit FAK and IGF-1R decreases growth of pancreatic cancer xenografts. Mol. Carcinog., 2010, 49(2), 200-209.
13. Tognon, C.E.; Sorensen, PH. Targeting the insulin-like growth factor 1 receptor (IGF1R) signaling pathway for cancer therapy. Expert Opin. Ther. Targets, 2012, 16(1), 33-48.
14. Yang, J.; Ylipää, A.; Sun, Y.; Zheng, H.; Chen, K.; Nykter, M.; Trent, J.; Ratner, N.; Lev, D.C.; Zhang, W. Genomic and molecular characterization of malignant peripheral nerve sheath tumor identifies the IGF1R pathway as a primary target for treatment. Clin. Cancer Res., 2011, 17(24), 7563-7573.
15. McLean, G.W.; Carragher, N.O.; Avizienyte, E.; Evans, J.; Brunton, V.G.; and Frame, M.C. The role of focal-adhesion kinase in cancer - a new therapeutic opportunity. Nat. Rev. Cancer, 2005, 5(7), 505-515.
16. Hochwald, S.N.; Golubovskaya, V. FAK as a target for cancer therapy. Gene Ther. Mol. Biol., 2009, 13, 26-35.
17. Ucar, D.A.; Dang, L.; Hochwald, S.N. FAK signaling and function in pancreatic cancer. Frontiers in Bioscience, 2011, 3(1), 750-756.
18. Frame, M.C.; Patel, H.; Serrels, B.; Lietha, D.; Eck, M.J. The FERM domain: organizing the structure and function of FAK. Nat.Rev. Mol. Cell Biol., 2010, 11(11), 802-814.
19. Ucar, D.A.; Hochwald, S.N. FAK and interacting proteins as therapeutic targets in pancreatic cancer. Anti-Cancer Agents in Med. Chem., 2010, 10 (10), 742-746.
20. Ucar, D.; Hochwald, S.N. FAK as a therapeutic target in malignancy. Recent Adv. in Carcinogenesis, 2010, 1, 1-7.
21. Kurenova, E.V.; Hunt, D.L.; He, D.; Magis, A.T.; Ostrov, D.A.; and Cance, W.G. Small molecule chloropyramine hydrochloride (C4) targets the binding site of focal adhesion kinase and vascular endothelial growth factor receptor 3 and suppresses breast cancer growth in vivo. J. Med. Chem., 2009, 52(15), 4716-4724.
22. Ucar, D.A.; Cox, A.; He, D.H.; Ostrov, D.A.; Kurenova, E.; Hochwald, S.N. A novel small molecule inhibitor of FAK and IGF- 1R protein interactions decreases growth of human esophageal carcinoma. Anticancer Agents Med. Chem., 2011, 11 (7), 629-37.
23. Chen, T.H.; Chan, P.C.; Chen, C.L.; Chen, H.C. Phosphorylation of focal adhesion kinase on tyrosine 194 by Met leads to its activation through relief of autoinhibition. Oncogene, 2011, 30 (2), 153-166.
24. Roberts, W.G.; Ung, E.; Whalen, P.; Cooper, B.; Hulford, C.; Autry, C.; Richter, D.; Emerson, E.; Lin, J.; Kath, J.; Coleman, K.; Yao, L.; Martinez-Alsina, L.; Lorenzen, M.; Berliner, M.; Luzzio, M.; Patel, N.; Schmitt, E.; LaGreca, S.; Jani, J.; Wessel, M.; Marr, E.; Griffor, M.; and Vajdos, F. Antitumor activity and pharmacology of a selective focal adhesion kinase inhibitor, PF- 562,271. Cancer Res., 2008, 68(6), 1935-1944.
25. Zhang, J.; Yang, P.L.; Gray, N.S. Targeting cancer with small molecule kinase inhibitors. Nat. Rev. Cancer, 2009, 9, 28-39.
26. Watanabe, N.; Takaoka, M.; Sakurama, K.; Tomono, Y.; Hatakeyama, S.; Ohmori, O.; Motoki, T.; Shirakawa, Y.; Yamatsuji, T.; Haisa, M.; Matsuoka, J.; Beer, D.G.; Nagatsuka, H.; Tanaka, N.; Naomoto, Y. Dual tyrosine kinase inhibitor for focal adhesion kinase and insulin-like growth factor-I receptor exhibits anticancer effect in esophageal adenocarcinoma in vitro and in vivo. Clin. Cancer Res., 2008, 14(14), 4631-4639.
27. Zheng, D.; Kurenova, E.; Ucar, D.; Golubovskaya, V.; Magis, A.; Ostrov, D.; Cance, W.G.; and Hochwald, S.N. Targeting of the protein interaction site between FAK and IGF-1R. Biochem. Biophys. Res. Commun., 2009, 388 (2), 301-305.
28. Sieg, D.J.; Hauck, C.R.; Ilic, D.; Klingbeil, C.K.; Schaefer, E.;Damsky, C.H.; Schlaepfer, D.D. FAK integrates growth-factor and integrin signals to promote cell migration. Nat. Cell. Biol., 2000, 2 (5), 249-256.
29. Hall, J.E.; Fu, W.; Schaller, M.D. Focal adhesion kinase: exploring Fak structure to gain insight into function. Int. Rev. Cell. Mol. Biol., 2011, 288, 185-225.
30. Ucar, D.A.; Kurenova, E.; Garrett, T.J.; Cance, W.G.; Nyberg, C.; Cox, A.; Massoll, N.; Ostrov, D.; Lawrence, N.; Sebti, S.; Zajac-Kaye, M.; Hochwald, S.N. Disruption of the protein interaction of FAK and IGF-1R inhibits melanoma tumor growth. Cell Cycle, 2012, 11(17), 3250-3259.
31. Kurenova, E.; Xu, L.H.; Yang, X.; Baldwin, A.S Jr.; Craven, R.J.; Hanks, S.K.; Liu, Z.G.; Cance, W.G. Focal adhesion kinase suppresses apoptosis by binding to the death domain of receptorinteracting protein. Mol. Cell Biol., 2004, 24(10), 4361-4371.