Subtype-specific MEK-PI3 kinase feedback as a therapeutic target in pancreatic adenocarcinoma

Molecular Cancer Therapeutics

Volumn 12, Issue 10, 2013, Pages 2213-2225

  Mirzoeva, Olga K ^a   Collisson, Eric A ^b,c   Schaefer, Peter M ^a   Hann, Byron ^c   Hom, Yun K ^c   Ko, Andrew H ^b,c   Korn, W Michael ^a,b,c  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

2 (2 CHLORO 4 IODOANILINO) N CYCLOPROPYLMETHOXY 3,4 DIFLUOROBENZAMIDE; BETA ACTIN; EPIDERMAL GROWTH FACTOR RECEPTOR; EPIDERMAL GROWTH FACTOR RECEPTOR KINASE INHIBITOR; ERLOTINIB; MICRORNA; MICRORNA 200; MITOGEN ACTIVATED PROTEIN KINASE INHIBITOR; MITOGEN ACTIVATED PROTEIN KINASE KINASE; ONCOPROTEIN; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN HER3; PROTEIN KINASE B; TRANSCRIPTION FACTOR ZEB1; UNCLASSIFIED DRUG; UVOMORULIN;

APOPTOSIS; ARTICLE; CANCER CELL CULTURE; CONTROLLED STUDY; DRUG POTENTIATION; ENZYME INHIBITION; EPITHELIUM CELL; FEEDBACK SYSTEM; GENE EXPRESSION; GENE MUTATION; HUMAN; HUMAN CELL; MESENCHYME CELL; MULTIGENE FAMILY; ONCOGENE K RAS; PANCREAS ADENOCARCINOMA; PRIORITY JOURNAL; RNA ANALYSIS; SENSITIZATION;

ADENOCARCINOMA; APOPTOSIS; CELL LINE, TUMOR; FEEDBACK, PHYSIOLOGICAL; HOMEODOMAIN PROTEINS; HUMANS; MAP KINASE KINASE KINASES; MICRORNAS; MOLECULAR TARGETED THERAPY; PANCREATIC NEOPLASMS; PHOSPHATIDYLINOSITOL 3-KINASES; PROTO-ONCOGENE PROTEINS; RAS PROTEINS; RECEPTOR, EPIDERMAL GROWTH FACTOR; RNA, SMALL INTERFERING; TRANSCRIPTION FACTORS;

EID: 84885642998     PISSN: 15357163     EISSN: 15388514     Source Type: Journal    
DOI: 10.1158/1535-7163.MCT-13-0104     Document Type: Article

References (40)

1. Conroy T, Desseigne F, Ychou M, Bouche O, Guimbaud R, Becouarn Y, et al. FOLFIRINOX versus gemcitabine for metastatic pancreatic cancer. N Engl J Med 2011;364: 1817-25.
2. Von Hoff DD, Ramanathan RK, Borad MJ, Laheru DA, Smith LS, Wood TE, et al. Gemcitabine plus nab-paclitaxel is an active regimen in patients with advanced pancreatic cancer: a phase I/II trial. J Clin Oncol 2011;29: 4548-54.
3. Almoguera C, Shibata D, Forrester K, Martin J, Arnheim N, Perucho M. Most human carcinomas of the exocrine pancreas contain mutant c-Kras genes. Cell 1988;53: 549-54.
4. Hingorani SR, Wang L, Multani AS, Combs C, Deramaudt TB, Hruban RH, et al. Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. Cancer Cell 2005;7: 469-83.
5. Downward J. Targeting RAS signalling pathways in cancer therapy. Nat Rev Cancer 2003;3: 11-22.
6. Chadha KS, Khoury T, Yu J, Black JD, Gibbs JF, Kuvshinoff BW, et al. Activated Akt and Erk expression and survival after surgery in pancreatic carcinoma. Ann Surg Oncol 2006;13: 933-9.
7. Young A, Lyons J, Miller AL, Phan VT, Alarcon IR, McCormick F. Ras signaling and therapies. Adv Cancer Res 2009;102: 1-17.
8. Repasky GA, Chenette EJ, Der CJ. Renewing the conspiracy theory debate: does Raf function alone to mediate Ras oncogenesis? Trends Cell Biol 2004;14: 639-47.
9. Moore MJ, Goldstein D, Hamm J, Figer A, Hecht JR, Gallinger S, et al. Erlotinib plus gemcitabine compared with gemcitabine alone in patients with advanced pancreatic cancer: a phase III trial of the National Cancer Institute of Canada Clinical Trials Group. J Clin Oncol 2007;25: 1960-6.
10. Rinehart J, Adjei AA, Lorusso PM, Waterhouse D, Hecht JR, Natale RB, et al. Multicenter phase II study of the oral MEK inhibitor, CI-1040, in patients with advanced non-small-cell lung, breast, colon, and pancreatic cancer. J Clin Oncol 2004;22: 4456-62.
11. Patnaik A, LoRusso P, Tabernero JA, Laird D, Aggarwal S, Papadopoulos K. Biomarker development for XL765, a potent and selective oral dual inhibitor of PI3K and mTOR currently being administered to patients in a Phase I clinical trial. Molecular Targets and Cancer Therapeutics Conference. San Francisco; 2007. p. B265.
12. Collisson EA, Sadanandam A, Olson P, Gibb WJ, Truitt M, Gu S, et al. Subtypes of pancreatic ductal adenocarcinoma and their differing responses to therapy. Nat Med 2011;17: 500-3.
13. Sun SY, Rosenberg LM, Wang X, Zhou Z, Yue P, Fu H, et al. Activation of Akt and eIF4E survival pathways by rapamycin-mediated mammalian target of rapamycin inhibition. Cancer Res 2005; 65: 7052-8.
14. O'Reilly KE, Rojo F, She QB, Solit D, Mills GB, Smith D, et al. mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt. Cancer Res 2006;66: 1500-8.
15. Mirzoeva OK, Das D, Heiser LM, Bhattacharya S, Siwak D, Gendelman R, et al. Basal subtype andMAPK/ERK kinase (MEK)-phosphoinositide 3-kinase feedback signaling determine susceptibility of breast cancer cells to MEK inhibition. Cancer Res 2009;69: 565-72.
16. Jimeno A, Rubio-Viqueira B, Amador ML, Grunwald V, Maitra A, Iacobuzio-Donahue C, et al. Dual mitogen-activated protein kinase and epidermal growth factor receptor inhibition in biliary and pancreatic cancer. Mol Cancer Ther 2007;6: 1079-88.
17. Diep CH, Munoz RM, Choudhary A, Von Hoff DD, Han H. Synergistic effect between erlotinib and MEK inhibitors in KRAS wild-type human pancreatic cancer cells. Clin Cancer Res 2011;17: 2744-56.
18. Gysin S, Rickert P, Kastury K, McMahon M. Analysis of genomic DNA alterations and mRNA expression patterns in a panel of human pancreatic cancer cell lines. Genes Chromosomes Cancer 2005;44: 37-51.
19. Chou TC, Talalay P. Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors. Adv Enzyme Regul 1984;22: 27-55.
20. Smyth GK. Limma: linear models for microarray data. In:Gentleman R, Carey V, Dudoit S, Irizarry R, Huber W, editors. Bioinformatics and Computational Biology Solutions using R and Bioconductor. New York: Springer; 2005. p. 397-420.
21. Gentleman RC, Carey VJ, Bates DM, Bolstad B, Dettling M, Dudoit S, et al. Bioconductor: open software development for computational biology and bioinformatics. Genome Biol 2004;5:R80.
22. Dabney A, Storey J, Warnes G. qvalue: Q-value estimation for false discovery rate control R package version 1.24.0. 2010. Available from: http://CRAN.R-project.org/package=qvalue.
23. Hastie T, Tibshirani R, Narasimhan B, Chu G. 2009. PAMR: PAM: Prediction Analysis for Microarrays. R Package Version 1.33. Available from: http://cran.r-project.org/package=pamr.
24. Team RDC. R: a language and environment for statistical computing. Vienna, Austria: R Foundation for Statistical Computing; 2010.
25. Burk U, Schubert J, Wellner U, Schmalhofer O, Vincan E, Spaderna S, et al. A reciprocal repression between ZEB1 and members of the miR- 200 family promotes EMT and invasion in cancer cells. EMBO Rep 2008;9: 582-9.
26. Gregory PA, Bert AG, Paterson EL, Barry SC, Tsykin A, Farshid G, et al. The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1. Nat Cell Biol 2008; 10: 593-601.
27. Peinado H, Olmeda D, Cano A. Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype? Nat Rev Cancer 2007;7: 415-28.
28. Bracken CP, Gregory PA, Kolesnikoff N, Bert AG, Wang J, Shannon MF, et al. A double-negative feedback loop between ZEB1-SIP1 and the microRNA-200 family regulates epithelial-mesenchymal transition. Cancer Res 2008;68: 7846-54.
29. Lacher MD, Shiina M, Chang P, Keller D, Tiirikainen MI, Korn WM. ZEB1 limits adenoviral infectability by transcriptionally repressing the coxsackie virus and adenovirus receptor. Mol Cancer 2011; 10:91.
30. Flaherty KT, Robert C, Hersey P, Nathan P, Garbe C, Milhem M, et al. Improved survival with MEK inhibition in BRAF-mutated melanoma. N Engl J Med 2012;367: 107-14.
31. Collisson EA, Trejo CL, Silva JM, Gu S, Korkola JE, Heiser LM, et al. A central role for RAF!MEK!ERK signaling in the genesis of pancreatic ductal adenocarcinoma. Cancer Discov 2012;2: 685-93.
32. Gysin S, Paquette J, McMahon M. Analysis of mRNA expression profiles after MEK1/2 inhibition reveals pathways involved in drug sensitivity. Mol Cancer Res 2012;10: 1607-19.
33. Garraway LA, Janne PA. Circumventing cancer drug resistance in the era of personalized medicine. Cancer Discov 2012;2: 214-26.
34. Chandarlapaty S, Sawai A, Scaltriti M, Rodrik-Outmezguine V, Grbovic-Huezo O, Serra V, et al. AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity. Cancer Cell 2011;19: 58-71.
35. Soltoff SP, Carraway KL III, Prigent SA, Gullick WG, Cantley LC. ErbB3 is involved in activation of phosphatidylinositol 3-kinase by epidermal growth factor. Mol Cell Biol 1994;14: 3550-8.
36. Sergina NV, Rausch M, Wang D, Blair J, Hann B, Shokat KM, et al. Escape from HER-family tyrosine kinase inhibitor therapy by the kinase-inactive HER3. Nature 2007;445: 437-41.
37. Buck E, Eyzaguirre A, Barr S, Thompson S, Sennello R, Young D, et al. Loss of homotypic cell adhesion by epithelial-mesenchymal transition or mutation limits sensitivity to epidermal growth factor receptor inhibition. Mol Cancer Ther 2007;6: 532-41.
38. Thomson S, Buck E, Petti F, Griffin G, Brown E, Ramnarine N, et al. Epithelial to mesenchymal transition is a determinant of sensitivity of non-small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition. Cancer Res 2005;65: 9455-62.
39. Bryant JL, Britson J, Balko JM, Willian M, Timmons R, Frolov A, et al. A microRNA gene expression signature predicts response to erlotinib in epithelial cancer cell lines and targets EMT. Br J Cancer 2012;106: 148-56.
40. Witta SE, Dziadziuszko R, Yoshida K, Hedman K, Varella-Garcia M, Bunn PA Jr, et al. ErbB-3 expression is associated with E-cadherin and their coexpression restores response to gefitinib in non-small-cell lung cancer (NSCLC). Ann Oncol 2009;20: 689-95.