TRPV2 channel negatively controls glioma cell proliferation and resistance to Fas-induced apoptosis in ERK-dependent manner

Carcinogenesis

Volumn 31, Issue 5, 2010, Pages 794-803

  Nabissi, Massimo ^a   Morelli, Maria Beatrice ^a,b   Amantini, Consuelo ^a   Farfariello, Valerio ^a,b   Ricci Vitiani, Lucia ^c   Caprodossi, Sara ^a   Arcella, Antonella ^d   Santoni, Matteo ^a   Giangaspero, Felice ^d   De Maria, Ruggero ^c   Santoni, Giorgio ^a  

^a UNIVERSITY OF CAMERINO   (Italy)

^b SAPIENZA UNIVERSITY OF ROME   (Italy)

^c ISTITUTO SUPERIORE DI SANITÀ   (Italy)

^d IRCCS NEUROMED   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

CYCLIN DEPENDENT KINASE 2; CYCLIN E; FAS ANTIGEN; MESSENGER RNA; PROCASPASE 8; PROTEIN BCL XL; TRANSCRIPTION FACTOR E2F1; VANILLOID RECEPTOR 2; 2 (2 AMINO 3 METHOXYPHENYL)CHROMONE; BCL2L1 PROTEIN, HUMAN; FLAVONOID; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN BCL X; PROTEIN KINASE B; TRPV2 PROTEIN, HUMAN; VANILLOID RECEPTOR;

ARTICLE; CANCER GRADING; CELL DIFFERENTIATION; CELL PROLIFERATION; CELL VIABILITY; CONTROLLED STUDY; DOWN REGULATION; GENE EXPRESSION; GENE FUNCTION; GENE SILENCING; GLIOMA CELL; HUMAN; HUMAN CELL; HUMAN TISSUE; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; REAL TIME POLYMERASE CHAIN REACTION; SENSITIVITY ANALYSIS; SIGNAL TRANSDUCTION; UPREGULATION; WESTERN BLOTTING; APOPTOSIS; DRUG ANTAGONISM; GENETICS; GLIOMA; METABOLISM; PATHOLOGY; PHOSPHORYLATION; PHYSIOLOGY; TUMOR CELL LINE;

ANTIGENS, CD95; APOPTOSIS; BCL-X PROTEIN; CELL LINE, TUMOR; CELL PROLIFERATION; EXTRACELLULAR SIGNAL-REGULATED MAP KINASES; FLAVONOIDS; GLIOMA; HUMANS; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; RNA, MESSENGER; TRPV CATION CHANNELS;

EID: 77952296263     PISSN: 01433334     EISSN: 14602180     Source Type: Journal    
DOI: 10.1093/carcin/bgq019     Document Type: Article

References (50)

1. Kleihues, P. et al. (2002) The WHO classification of tumors of the nervous system. J. Neuropathol. Exp. Neurol., 61, 215-225.
2. Giese, A. et al. (1996) Glioma invasion in the central nervous system. Neurosurgery, 39, 235-250.
3. Castro, M.G. et al. (2003) Current and future strategies for the treatment of malignant brain tumors. Pharmacol. Ther., 98, 71-108.
4. Ashkenazi, A. et al. (1998) Death receptors: signaling and modulation. Science, 281, 1305-1308.
5. Scaffidi, C. et al. (1998) Two CD95 (APO/Fas) signaling pathways. EMBO J., 16, 1675-1687.
6. Holmström, T.H. et al. (2000) MAPK/ERK signalling in activated T cells inhibits CD95/Fas-mediated apoptosis downstream of DISC assembly. EMBO J., 19, 5418-5428.
7. Söderström, T.S. et al. (2002) Mitogen-activated protein kinase/extracellular signal-regulated kinase signaling in activated T cells abrogates TRAIL-induced apoptosis upstream of the mitochondrial amplification loop and caspase-8. J. Immunol., 169, 2851-2860.
8. Cagnol, S. et al. (2006) Prolonged activation of ERK 1, 2 induces FADD-independent caspase 8 activation and cell death. Apoptosis, 11, 337-346.
9. Fanton, C.P. et al. (2001) Dual growth arrest pathways in astrocytes and astrocytic tumors in response to Raf-1 activation. J. Biol. Chem., 276, 18871-18877.
10. Marshall, C.J. (1994) MAP kinase kinase kinase, MAP kinase kinase and MAP kinase. Curr. Opin. Genet. Dev., 4, 82-89.
11. Bonni, A. et al. (1999) Cell survival promoted by the Ras-MAPK signalling pathway by transcription-dependent and -independent mechanisms. Science, 286, 1358-1362.
12. Erhardt, P. et al. (1999) B-Raf inhibits programmed cell death downstream of cytochrome c release from mitochondria by activating the MEK/Erk pathway. Mol. Cell. Biol, 19, 5308-5315.
13. Wilson, D.J. et al. (1999) MEK1 activation rescues Jurkat T cells from Fas-induced apoptosis. Cell. Immunol., 194, 67-77.
14. Bödding, M. (2007) TRP proteins and cancer. Cell Signal, 19, 617-624.
15. Prevarskaya, N. et al. (2007) TRP channels in cancer. Biochim. Biophys. Acta, 1772, 937-946.
16. Amantini, C. et al. (2007) Capsaicin-induced apoptosis of glioma cells is mediated by TRPV1 vanilloid receptor and requires p38 MAPK activation. J. Neurochem, 102, 977-990.
17. Caterina, M.J. et al. (1999) A capsaicin-receptor homologue with a high threshold for noxious heat. Nature, 398, 436-441.
18. Muraki, K. et al. (2003) TRPV2 is a component of osmotically sensitive cation channels in murine aortic myocytes. Circ. Res., 93, 829-838.
19. Zimmermann, K. et al. (2005) The TRPV1/2/3 activator 2-aminoethoxydiphenyl borate sensitizes native nociceptive neurons to heat in wild type but not TRPV1 deficient mice. Neuroscience, 135, 1277-1284.
20. Qin, N. et al. (2008) TRPV2 is activated by cannabidiol and mediates CGRP release in cultured rat dorsal root ganglion neurons. J. Neurosci., 28, 6231-6238.
21. Kowase, T. et al. (2002) Immunohistochemical localization of growth factor-regulated channel (GRC) in human tissues. Endocr. J., 49, 349-355.
22. Saunders, C.I. et al. (2007) Expression of transient receptor potential vanilloid 1 (TRPV1) and 2 (TRPV2) in human peripheral blood. Mol. Immunol., 44, 1429-1435.
23. Caprodossi, S. et al. (2008) Transient receptor potential vanilloid type 2 (TRPV2) expression in normal urothelium and in urothelial carcinoma of human bladder: correlation with the pathologic stage. Eur. Urol., 54, 612-620.
24. Kanzaki, M. et al. (1999) Translocation of a calcium-permeable cation channel induced by insulin-like growth factor-I. Nat. Cell Biol, 1, 165-170.
25. Penna, A. et al. (2006) PI3-kinase promotes TRPV2 activity independently of channel translocation to the plasma membrane. Cell Calcium, 39, 495-507.
26. 2+-permeable growth factor-related channel. J. Cell Biol., 161, 957-967.
27. Monet, M. et al. (2009) Lysophospholipids stimulate prostate cancer cell migration via TRPV2 channel activation. Biochim. Biophys. Acta., 1793, 528-539.
28. Mandell, J.W. et al. (1998) In situ visualization of intratumor growth factor signaling: immunohistochemical localization of activated ERK/MAP kinase in glial neoplasms. Am. J. Pathol., 153, 1411-1423.
29. Pardo, O.E. et al. (2002) Fibroblast growth factor-2 induces translational regulation of Bcl-XL and Bcl-2 via a MEK-dependent pathway. J. Biol. Chem., 277, 12040-12046.
30. Lee, J.T. et al. (2007) Akt inactivates ERK causing decreased response to chemotherapeutic drugs in advanced CaP cells. Cell Cycle, 7, 631-636.
31. Manning, B.D. et al. (2007) AKT/PKB signaling: navigating downstream. Cell, 129, 1261-1274.
32. Yount, G.L., Levine, K.S., Kuriyama, H., Haas-Kogan, D.A. and Israel, M.A. (1999) Fas (APO-1/CD95) signalling pathway is intact in radioresistant human glioma cells. Cancer Res., 59, 1362-1365.
33. Nagane, M. et al. (1998) Drug resistance of human glioblastoma cells conferred by a tumor-specific mutant epidermal growth factor receptor through modulation of Bcl-XL and caspase-3-like proteases. Proc. Natl Acad. Sci. USA, 10, 5274-5279.
34. Mcferrin, M.B. et al. (2006) A role for ion channels in glioma invasion. Neuron Glia Biol., 2, 39-49.
35. Huang, L. et al. (2009) ATP-sensitive potassium channels control glioma cells proliferation by regulating ERK activity. Carcinogenesis, 30, 737-744.
36. Katsetos, C.D. et al. (2003) Class III beta-tubulin isotype: a key cytoskeletal protein at the crossroads of developmental neurobiology and tumor neuropathology. J. Child Neurol., 18, 851-866.
37. Giraud, S. et al. (2007) In vitro apoptotic introduction of human glioblastoma cells by Fas ligand plus etoposide and in vivo antitumour activity of combined drugs in xenografted nude rats. Int. J. Oncol., 30, 273-281.
38. Shaul, Y.D. et al. (2007) The MEK/ERK cascade from signaling specificity to diverse functions. Biochim. Biophys. Acta., 1773, 1213-1226.
39. Walker, L.S. et al. (1999) Lack of activation induced cell death in human T blast despite CD95L up-regulation: protection from apoptosis by MEK signalling. Immunology, 98, 569-575.
40. Kalas, W. et al. (2002) Inhibition of MEK induces Fas expression and apoptosis in lymphomas overexpressing Ras. Leuk. Lymphoma, 43, 1469-1474.
41. Lind, C.R. et al. (2006) The mitogen-activated/extracellular signal-regulated kinase kinase 1/2 inhibitor U0126 induces glial fibrillary acid protein expression and reduces the proliferation and migration of C6 glioma cells. Neuroscience, 141, 1925-1933.
42. Boesen-de Cock, J.G. et al. (1998) The anti-cancer drug etoposide can induce caspase-8 processing and apoptosis in absence of CD95 receptor-ligand interaction. Apoptosis, 3, 17-25.
43. Röhn, T.A. et al. (2001) CCNU-dependent potentiation of TRAIL/Apo2L-induced apoptosis in human glioma cells is p53-independent but may involve enhanced cytochrome c release. Oncogene, 20, 4128-4137.
44. Roos, W. et al. (2004) Apoptosis triggered by DNA damage 06-methylguanine in human lymphocytes requires DNA replication and is mediated by p53 and Fas/CD95/Apo-1. Oncogene, 23, 359-367.
45. Decaudin, D. et al. (1997) Bcl-2 and Bcl-XL antagonize the mitochondrial dysfunction preceding nuclear apoptosis induced by chemotherapeutic agents. Cancer Res., 57, 62-67.
46. Jost, M. et al. (2001) Epidermal growth factor receptor-dependent control of keratinocyte survival and Bcl-xL expression through a MEK-dependent pathway. J. Biol. Chem., 276, 6320-6326.
47. Feng, H. et al. (2004) Evidence for a novel caspase-8-independent, Fas death domain-mediated apoptotic pathway. J. Biomed. Biotechnol., 2004, 41-51.
48. Zhang, L. et al. (2004) A caspase-8-independent signalling pathway activated by Fas ligation leads to exposure of the Bak N terminus. J. Biol. Chem., 279, 33865-33874.
49. Luo, X. et al. (1998) Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors. Cell, 94, 481-490.
50. Belka, C. et al. (2000) Differential role of caspase-8 and BID activation during radiation-and CD95-induced apoptosis. Oncogene, 19, 1181-1190.