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Department of Neuro-Oncology and The Brain Tumor Center [M. A. D., T. S., P. T., D. K., W. K. A. Y., P. A. S.] and Department of Molecular Oncology [Y. L., X. F., R. L., G. B. M.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030; Canji Inc., San Diego, California 92121 [R. B.]; and Cancer Research Institute, University of California, San Francisco, California 94115 [D. S.]
The MMAC/PTEN tumor suppressor gene encodes for a phosphatase that recently has been shown to have phosphotidylinositol phosphatase activity, implicating its possible involvement in phosphatidylinositol 3'-kinase-mediated signaling. To investigate possible alterations in growth factor-mediated signal transduction, an adenovirus containing MMAC/PTEN, Ad-MMAC, previously shown to inhibit growth and tumorigenicity in glioma cells, was used to acutely express the transgene. Human glioma cells infected with Ad-MMAC but not with control adenoviruses exhibited an inhibition of phosphorylation of both activating residues of Akt, Ser-473, and Thr-308, along with Akt's serine/threonine kinase activity, without significantly altering Akt expression. The effects of functional MMAC/PTEN expression were relatively specific, because members of several other growth factor-mediated signaling pathways showed no altered responses. The presence of MMAC/PTEN also inhibited phosphorylation of BAD, although no evidence of apoptosis in the in situ treated cells was observed. However, U251 glioma cells infected with Ad-MMAC were induced to undergo anoikis at a significantly higher rate than U251 cells treated with control viruses or mock infected with media. These results demonstrate that the acute administration of MMAC/PTEN results in the inhibition of Akt-mediated signaling, growth inhibition, and anoikis, implying that loss of MMAC/PTEN increases cellular proliferation and significantly augments a cell's survival potential during cellular processes that are associated with malignancy.
1 Supported by NIH Grants CA56041 and CA55261, State of Texas Advanced Technology Program Grant 97-110, and the Pediatric Brain Tumor Foundation (to P. A. S.) and NIH Grant CA71418 (to G. B. M.).
2 The first two authors contributed equally to this work.
3 To whom requests for reprints should be addressed, at Department of Neuro-Oncology, The University of Texas M. D. Anderson Cancer Center, Box 316, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: (713) 792-3003; Fax: (713) 745-1183; E-mail: steckpa@audumla.mdacc.tmc.edu.
Received 8/20/98. Accepted 10/16/98.
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N. B. Adey, L. Huang, P. A. Ormonde, M. L. Baumgard, R. Pero, D. V. Byreddy, S. V. Tavtigian, and P. L. Bartel Threonine Phosphorylation of the MMAC1/PTEN PDZ Binding Domain Both Inhibits and Stimulates PDZ Binding Cancer Res., January 1, 2000; 60(1): 35 - 37. [Abstract] [Full Text]
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M. E. McMenamin, P. Soung, S. Perera, I. Kaplan, M. Loda, and W. R. Sellers Loss of PTEN Expression in Paraffin-embedded Primary Prostate Cancer Correlates with High Gleason Score and Advanced Stage Cancer Res., September 1, 1999; 59(17): 4291 - 4296. [Abstract] [Full Text] [PDF]
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K. Nakatani, D. A. Thompson, A. Barthel, H. Sakaue, W. Liu, R. J. Weigel, and R. A. Roth Up-regulation of Akt3 in Estrogen Receptor-deficient Breast Cancers and Androgen-independent Prostate Cancer Lines J. Biol. Chem., July 30, 1999; 274(31): 21528 - 21532. [Abstract] [Full Text] [PDF]
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M. A. Davies, D. Koul, H. Dhesi, R. Berman, T. J. McDonnell, D. McConkey, W. K. A. Yung, and P. A. Steck Regulation of Akt/PKB Activity, Cellular Growth, and Apoptosis in Prostate Carcinoma Cells by MMAC/PTEN Cancer Res., June 1, 1999; 59(11): 2551 - 2556. [Abstract] [Full Text] [PDF]
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I. W. Cheney, S. T. C. Neuteboom, M.-T. Vaillancourt, M. Ramachandra, and R. Bookstein Adenovirus-mediated Gene Transfer of MMAC1/PTEN to Glioblastoma Cells Inhibits S Phase Entry by the Recruitment of p27Kip1 into Cyclin E/CDK2 Complexes Cancer Res., May 1, 1999; 59(10): 2318 - 2323. [Abstract] [Full Text] [PDF]
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D. Koul, Y. Yao, J. L. Abbruzzese, W. K. A. Yung, and S. A. G. Reddy Tumor Suppressor MMAC/PTEN Inhibits Cytokine-induced NFkappa B Activation without Interfering with the Ikappa B Degradation Pathway J. Biol. Chem., March 30, 2001; 276(14): 11402 - 11408. [Abstract] [Full Text] [PDF]
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