Inhibition of PI3K/AKT/mTOR pathway enhances temozolomide-induced cytotoxicity in pituitary adenoma cell lines in vitro and xenografted pituitary adenoma in female nude mice

Endocrinology

Volumn 154, Issue 3, 2013, Pages 1247-1259

  Dai, Congxin ^a   Zhang, Bo ^b   Liu, Xiaohai ^a   Ma, Sihai ^a   Yang, Yakun ^a   Yao, Yong ^a   Feng, Ming ^a   Bao, Xinjie ^a   Li, Guilin ^a   Wang, Janxin ^a   Guo, Kai ^b   Ma, Wenbin ^a   Xing, Bing ^a   Lian, Wei ^a   Xiao, Jianqi ^a   Cai, Feng ^a   Zhang, Hongbin ^c   Wang, Renzhi ^a  

^a PEKING UNION MEDICAL COLLEGE HOSPITAL   (China)

^b Medical University   (China)

^c INSTITUTE OF BASIC MEDICAL SCIENCES   (China)

Author keywords

[No Author keywords available]

Indexed keywords

CASPASE 3; CASPASE 7; GROWTH HORMONE; MAMMALIAN TARGET OF RAPAMYCIN; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; PHOSPHATIDYLINOSITOL 3 KINASE; PROLACTIN; PROTEIN BAX; PROTEIN BCL 2; PROTEIN KINASE B; TEMOZOLOMIDE; XL 765;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL LINE; CELL PROLIFERATION; CONTROLLED STUDY; CYTOTOXICITY; DRUG INHIBITION; DRUG MEGADOSE; DRUG POTENTIATION; ENZYME ACTIVITY; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; FEMALE; GROWTH HORMONE BLOOD LEVEL; HYPOPHYSIS ADENOMA; HYPOPHYSIS TUMOR; IN VITRO STUDY; IN VIVO STUDY; LOW DRUG DOSE; MOUSE; NONHUMAN; NUDE MOUSE; PRIORITY JOURNAL; PROLACTIN RELEASE; PROTEIN EXPRESSION; RANDOMIZED CONTROLLED TRIAL; TUMOR CELL; TUMOR GROWTH; TUMOR XENOGRAFT;

ADENOMA; ANIMALS; ANTINEOPLASTIC AGENTS, ALKYLATING; APOPTOSIS; CELL LINE, TUMOR; CELL PROLIFERATION; DACARBAZINE; DRUG SYNERGISM; DRUG THERAPY, COMBINATION; FEMALE; HUMAN GROWTH HORMONE; HUMANS; MICE; MICE, NUDE; PHOSPHATIDYLINOSITOL 3-KINASES; PITUITARY NEOPLASMS; PROLACTIN; PROTO-ONCOGENE PROTEINS C-AKT; QUINOXALINES; SIGNAL TRANSDUCTION; SULFONAMIDES; TOR SERINE-THREONINE KINASES; XENOGRAFT MODEL ANTITUMOR ASSAYS;

EID: 84874630091     PISSN: 00137227     EISSN: 19457170     Source Type: Journal    
DOI: 10.1210/en.2012-1908     Document Type: Article

References (47)

1. Asa SL, Ezzat S. The pathogenesis of pituitary tumours. Nat Rev Cancer. 2002;2:836-849.
2. Scheithauer BW, Kovacs KT, Laws EJ, Randall RV. Pathology of invasive pituitary tumors with special reference to functional classification. J Neurosurg. 1986;65:733-744.
3. Colao A, Grasso LF, Pivonello R, Lombardi G. Therapy of aggressive pituitary tumors. Expert Opin Pharmacother. 2011;12:1561-1570.
4. Hornyak M, Couldwell WT. Multimodality treatment for invasive pituitary adenomas. Postgrad Med. 2009;121:168-176.
5. Buchfelder M. Management of aggressive pituitary adenomas: Current treatment strategies. Pituitary. 2009;12:256-260.
6. Bei R, Marzocchella L, Turriziani M. The use of temozolomide for the treatment of malignant tumors: Clinical evidence and molecular mechanisms of action. Recent Pat Anticancer Drug Discov. 2010; 5:172-187.
7. Raverot G, Sturm N, de Fraipont F, et al. Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: A French multicenter experience. J Clin Endocrinol Metab. 2010;95:4592-4599.
8. Syro LV, Ortiz LD, Scheithauer BW, et al. Treatment of pituitary neoplasms with temozolomide: A review. Cancer. 2011;117:454-462.
9. Murakami M, Mizutani A, Asano S, et al.Amechanism of acquiring temozolomide resistance during transformation of atypical prolactinoma into prolactin-producing pituitary carcinoma: Case report. Neurosurgery. 2011;68:E1761-E1767.
10. Morin E, Berthelet F, Weisnagel J, Bidlingmaier M, Serri O. Failure of temozolomide and conventional doses of pegvisomant to attain biochemical control in a severe case of acromegaly. Pituitary. 2012; 15:97-100.
11. Losa M, Mazza E, Terreni MR, et al. Salvage therapy with temozolomide in patients with aggressive or metastatic pituitary adenomas: Experience in six cases. Eur J Endocrinol. 2010;163:843-851.
12. Shaw RJ, Cantley LC. Ras, PI(3)K and mTOR signalling controls tumour cell growth. Nature. 2006;441:424-430.
13. Liang J, Slingerland JM. Multiple roles of the PI3K/PKB (Akt) pathway in cell cycle progression. Cell Cycle. 2003;2:339-345.
14. Dworakowska D, Wlodek E, Leontiou CA, et al. Activation of RAF/ MEK/ERK and PI3K/AKT/mTOR pathways in pituitary adenomas and their effects on downstream effectors. Endocr Relat Cancer. 2009;16:1329-1338.
15. CakirM,Grossman AB. TargetingMAPK(Ras/ERK) and PI3K/Akt pathways in pituitary tumorigenesis. Expert Opin Ther Targets. 2009;13:1121-1134.
16. Lin Y, Jiang X, Shen Y, et al. Frequent mutations and amplifications of the PIK3CA gene in pituitary tumors. Endocr Relat Cancer. 2009; 16:301-310.
17. West KA, Castillo SS, Dennis PA. Activation of the PI3K/Akt pathway and chemotherapeutic resistance. Drug Resist Update. 2002; 5:234-248.
18. Molckovsky A, Siu LL. First-in-class, first-in-human phase I results of targeted agents: Highlights of the 2008 American Society of Clinical Oncology Meeting. J Hematol Oncol. 2008;1:20.
19. Prasad G, Sottero T, Yang X, et al. Inhibition of PI3K/mTOR pathways in glioblastoma and implications for combination therapy with temozolomide. Neuro-oncology. 2011;13:384-392.
20. Mirzoeva OK, Hann B, Hom YK, et al. Autophagy suppression promotes apoptotic cell death in response to inhibition of the PI3KmTOR pathway in pancreatic adenocarcinoma. J Mol Med (Berl). 2011;89:877-889.
21. Windle JJ, Weiner RI, Mellon PL. Cell lines of the pituitary gonadotrope lineage derived by targeted oncogenesis in transgenic mice. Mol Endocrinol. 1990;4:597-603.
22. Ostlund RJ, Leung JT, Hajek SV, Winokur T, Melman M. Acute stimulated hormone release from cultured GH3 pituitary cells. Endocrinology. 1978;103:1245-1252.
23. Judd AM, Login IS, Kovacs K, et al. Characterization of the MMQ cell, a prolactin-secreting clonal cell line that is responsive to dopamine. Endocrinology. 1988;123:2341-2350.
24. Bates RW, Garrison MM, Morris HP. Comparison of two different transplantable mammotropic pituitary tumors. Hormone content and effect on host. Proc Soc Exp Biol Med. 1966;123:67-70.
25. Liu Q, Sun JD, Wang J, et al. TH-302, a hypoxia-activated prodrug with broad in vivo preclinical combination therapy efficacy: Optimization of dosing regimens and schedules. Cancer Chemother Pharmacol. 2012;69:1487-1498.
26. Chou TC. Drug combination studies and their synergy quantification using the Chou-Talalay method. Cancer Res. 2010;70:440-446.
27. Goji K. Pulsatile characteristics of spontaneous growth hormone (GH) concentration profiles in boys evaluated by an ultrasensitive immunoradiometric assay: Evidence for ultradian periodicity ofGH secretion. J Clin Endocrinol Metab. 1993;76:667-670.
28. Ma S, Liu X, Yao Y, et al. Effect of temozolomide on cell viability in gonadotroph adenoma cell lines. Oncol Rep. 2011;26:543-550.
29. Sheehan J, Rainey J, Nguyen J, Grimsdale R, Han S. Temozolomideinduced inhibition of pituitary adenoma cells. J Neurosurg. 2011; 114:354-358.
30. Yasamura Y, Tashjian AJ, Sato GH. Establishment of four functional, clonal strains of animal cells in culture. Science. 1966;154: 1186-1189.
31. Heaney AP, FernandoM,MelmedS.PPAR-β receptor ligands: Novel therapy for pituitary adenomas. J Clin Invest. 2003;111:1381-1388.
32. Malla R, Gopinath S, Alapati K, et al. Downregulation of uPAR and cathepsin B induces apoptosis via regulation of Bcl-2 and Bax and inhibition of the PI3K/Akt pathway in gliomas. PLoS One. 2010; 5:e13731.
33. Li SL, Huang CH, Lin CC, et al. Antitumor effect of BPR-DC-2, a novel synthetic cyclic cyanoguanidine derivative, involving the inhibition of MDR-1 expression and down-regulation of p-AKT and PARP-1 in lung cancer. Invest New Drugs. 2011;29:195-206.
34. Musat M, Korbonits M, Kola B, et al. Enhanced protein kinase B/Akt signalling in pituitary tumours. Endocr Relat Cancer. 2005; 12:423-433.
35. Hoeflich KP, Merchant M, Orr C, et al. Intermittent administration of MEK inhibitor GDC-0973 plus PI3K inhibitor GDC-0941 triggers robust apoptosis and tumor growth inhibition. Cancer Res. 2012;72:210-219.
36. Roccaro AM, Sacco A, Husu EN, et al. Dual targeting of the PI3K/ Akt/mTOR pathway as an antitumor strategy in Waldenstrom macroglobulinemia. Blood. 2010;115:559-569.
37. Chandarlapaty S, Sawai A, Scaltriti M, et al. AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity. Cancer Cell. 2011;19:58-71.
38. Gomez-Pinillos A, Ferrari AC. mTOR signaling pathway and mTORinhibitors in cancer therapy. Hematol Oncol Clin NorthAm. 2012;26:483-505.
39. Park S, Zhao D, Hatanpaa KJ, et al. RIP1 activates PI3K-Akt via a dual mechanism involving NF-K B-mediated inhibition of the mTOR-S6K-IRS1 negative feedback loop and down-regulation of PTEN. Cancer Res. 2009;69:4107-4111.
40. Jouanneau E, Wierinckx A, Ducray F, et al. New targeted therapies in pituitary carcinoma resistant to temozolomide. Pituitary. 2012; 15:37-43.
41. Cerovac V, Monteserin-Garcia J, Rubinfeld H, et al. The somatostatin analogue octreotide confers sensitivity to rapamycin treatment on pituitary tumor cells. Cancer Res. 2010;70:666-674.
42. Hammond LA, Eckardt JR, Kuhn JG, et al. A randomized phase I and pharmacological trial of sequences of 1,3-bis(2-chloroethyl)-1-nitrosourea and temozolomide in patients with advanced solid neoplasms. Clin Cancer Res. 2004;10:1645-1656.
43. Roulin D, Waselle L, Dormond-Meuwly A, Dufour M, Demartines N, Dormond O. Targeting renal cell carcinoma with NVP-BEZ235, a dual PI3K/mTOR inhibitor, in combination with sorafenib. Mol Cancer. 2011;10:90.
44. Bhende PM, Park SI, Lim MS, Dittmer DP, Damania B. The dual PI3K/mTOR inhibitor, NVP-BEZ235, is efficacious against follicular lymphoma. Leukemia. 2010;24:1781-1784.
45. Fan QW, Weiss WA. Targeting the RTK-PI3K-mTOR axis in malignant glioma: Overcoming resistance. Curr Top Microbiol Immunol. 2010;347:279-296.
46. Hayakawa J, Ohmichi M, Tasaka K, et al. Regulation of the PRL promoter by Akt through cAMP response element binding protein. Endocrinology. 2002;143:13-22.
47. Sinnberg T, Lasithiotakis K, Niessner H, et al. Inhibition of PI3KAKT-mTOR signaling sensitizes melanoma cells to cisplatin and temozolomide. J Invest Dermatol. 2009;129:1500-1515.