p53-mediated inhibition of angiogenesis through up-regulation of a collagen prolyl hydroxylase

Science

Volumn 313, Issue 5789, 2006, Pages 968-971

  Teodoro, Jose G ^a   Parker, Albert E ^a   Zhu, Xiaochun ^a   Green, Michael R ^a  

^a UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CELLS; COLLAGEN; ENZYME KINETICS; ENZYMES; GENES; TUMORS;

ANGIOGENESIS; ANTIANGIOGENIC THERAPY; ENDOTHELIAL CELL; TUMOR GROWTH;

GENETIC ENGINEERING;

COLLAGEN TYPE 18; COLLAGEN TYPE 4; PROCOLLAGEN PROLINE 2 OXOGLUTARATE 4 DIOXYGENASE; PROTEIN P53;

ENZYME; GENE EXPRESSION; PHYSIOLOGICAL RESPONSE; PROTEIN; RODENT; TUMOR;

ANGIOGENESIS; ANIMAL EXPERIMENT; ARTICLE; CANCER INHIBITION; CELL GROWTH; COLLAGEN SYNTHESIS; CONTROLLED STUDY; ENDOTHELIUM CELL; ENZYME REGULATION; GENETIC LINKAGE; GROWTH INHIBITION; HUMAN; HUMAN CELL; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; REGULATORY MECHANISM; TRANSCRIPTION INITIATION;

ANGIOGENESIS INHIBITORS; ANIMALS; APOPTOSIS; AUTOANTIGENS; CELL LINE, TUMOR; COLLAGEN; COLLAGEN TYPE IV; COLLAGEN TYPE XVIII; ENDOSTATINS; ENDOTHELIAL CELLS; ENDOTHELIUM, VASCULAR; GENE EXPRESSION REGULATION, ENZYMOLOGIC; GENES, P53; HUMANS; MICE; MICE, NUDE; NEOPLASM TRANSPLANTATION; NEOPLASMS, EXPERIMENTAL; NEOVASCULARIZATION, PATHOLOGIC; NEOVASCULARIZATION, PHYSIOLOGIC; PEPTIDE FRAGMENTS; PROCOLLAGEN-PROLINE DIOXYGENASE; TRANSCRIPTION, GENETIC; TRANSPLANTATION, HETEROLOGOUS; TUMOR SUPPRESSOR PROTEIN P53; UP-REGULATION;

EID: 33747619857     PISSN: 00368075     EISSN: 10959203     Source Type: Journal    
DOI: 10.1126/science.1126391     Document Type: Article

References (19)

1. B. Vogelstein, D. Lane, A. J. Levine, Nature 408, 307 (2000).
2. Materials and methods are available as supporting material on Science Online.
3. W. S. el-Deiry et al., Cell 75, 817 (1993).
4. K. I. Kivirikko, R. Myllyla, Methods Enzymol. 82, 245 (1982).
5. In H1299 cells, collagen 18 appeared as a doublet, consistent with previous findings that the collagen 18 gene encodes two major splice variants in human cells (18).
6. The observed size difference between endogenous and ectopically expressed endostatin is primarily due to the ∼4-kD epitope tag present at the C terminus of the ectopically expressed collagen 18. In addition, sequence variation, as well as slight species differences in the site of proteolytic cleavage, may also contribute to small differences in electrophoretic mobility.
7. Y. Maeshima et al., Science 295, 140 (2002).
8. M. S. O'Reilly et al., Cell 88, 277 (1997).
9. Expression of vascular endothelial growth factor (VEGF) mas not affected by EDHB treatment (fig. 58) and therefore cannot explain the inability of CM from EDHB-treated, p53-expressing H1299 cells to induce apoptosis in HUVECs.
10. P. Carmeliet, R. K. Jain, Nature 407, 249 (2000).
11. P. Hainaut et al., Nucleic Acids Res. 25, 151 (1997).
12. I. J. Fidler, Cancer Res. 35, 218 (1975).
13. A. G. Marneros, B. R. Olsen, Matrix Biol. 20, 337 (2001).
14. R. Ravi et al., Genes Dev. 14, 34 (2000).
15. L. Zhang et al., Cancer Res. 60, 3655 (2000).
16. K. M. Dameron, O. V. Volpert, M. A. Tainsky, N. Bouck, Science 265, 1582 (1994).
17. M. Sund et al., Proc. Natl. Acad. Sci. U.S.A 102, 2934 (2005).
18. J. Saarela, R. Ylikarppa, M. Rehn, S. Purmonen, T. Pihlajaniemi, Matrix Biol. 16, 319 (1998).
19. We thank S. Benchimol for providing the plasmid pECH53; B. Vogelstein for the HCT116 cell lines; F. Graham for the adenovirus vectors Ad-LacZ, Ad-p53, and Ad-p53mut; B. Olsen for the collagen 18 cDNAs; and R. Kalluri for the antibody to tumstatin. We also thank members of the Green lab, both past and present, for useful discussions; C. Welch and 5. Griggs for technical assistance; and 5. Evans for editorial assistance. J.G.T. was supported by postdoctoral fellowships from the National Cancer Institute of Canada and the Medical Foundation Charles A. King Trust. M.R.G. is an investigator of the Howard Hughes Medical Institute.