Tumor hypoxia and the progression of prostate cancer

Current Urology Reports

Volumn 3, Issue 3, 2002, Pages 222-228

  Anastasiadis, Aristotelis G ^a   Stisser, Brian C ^a   Ghafar, Mohamed A ^a   Burchardt, Martin ^a   Buttyan, Ralph ^a  

^a Och Spine at New York Presbyterian Hospitals   (United States)

Author keywords

Prostate Cancer; Prostate Cancer Cell; Prostate Cancer Cell Line; Tumor Hypoxia; Vascular Endothelial Growth Factor Protein

Indexed keywords

DNA BINDING PROTEIN; HIF1A PROTEIN, HUMAN; HYPOXIA INDUCIBLE FACTOR 1; HYPOXIA INDUCIBLE FACTOR 1ALPHA; NUCLEAR PROTEIN; PHOSPHATIDYLINOSITOL 3 KINASE; TRANSCRIPTION FACTOR;

CELL HYPOXIA; DISEASE COURSE; GENE EXPRESSION REGULATION; HUMAN; MALE; METABOLISM; PATHOLOGY; PHYSIOLOGY; PROSTATE TUMOR; REVIEW;

1-PHOSPHATIDYLINOSITOL 3-KINASE; CELL HYPOXIA; DISEASE PROGRESSION; DNA-BINDING PROTEINS; GENE EXPRESSION REGULATION, NEOPLASTIC; HUMANS; HYPOXIA-INDUCIBLE FACTOR 1; HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT; MALE; NUCLEAR PROTEINS; PROSTATIC NEOPLASMS; TRANSCRIPTION FACTORS;

EID: 0036618197     PISSN: 15272737     EISSN: 15346285     Source Type: Journal    
DOI: 10.1007/s11934-002-0068-6     Document Type: Article

References (40)

1. Greenlee RT, Murray T, Bolden S, Wingo PA: Cancer statistics, 2000. CA Cancer J Clin 2000, 50:7–33. DOI: 10.3322/canjclin.50.1.7
2. Isaacs JT, Lundmo PI, Berges R, et al.: Androgen regulation of programmed death of normal and malignant prostatic cells. J Androl 1992, 13:457–64.
3. Buttyan R, Shabsigh A, Perlman H, Colombel M: Regulation of apoptosis in the prostate gland by androgenic steroids. Trends Endocrinol Metab 1999, 10:47–54. DOI: 10.1016/S1043-2760(98)00104-0
4. Shabsigh A, Ghafar MA, de la Taille A, et al.: Biomarker analysis demonstrates a hypoxic environment in the castrated rat ventral prostate gland. J Cell Biochem 2001, 81:437–444. DOI: 10.1002/1097-4644(20010601)81:3<437::AID-JCB1057>3.0.CO;2-6
5. Folkman J: Angiogenesis in cancer, vascular, rheumatoid, and other disease. Nat Med 1995, 1:27–31. DOI: 10.1038/nm0195-27
6. Semenza GL: Expression of hypoxia-inducible Factor 1: mechanisms and consequences. Biochem Pharmacol 2000, 59:47–53. Very well written review regarding structure, function, and signal transduction models of HIF-1, and its involvement in physiologic and pathologic conditions. DOI: 10.1016/S0006-2952(99)00292-0
7. Nordsmark M, Overgaard M, Overgaard J: Pretreatment oxygenation predicts radiation response in advanced squamous cell carcinoma of the head and neck. Radiother Oncol 1996, 41:31–39.
8. Hockel M, Schlenger K, Aral B, et al.: Association between tumor hypoxia and malignant progression in advanced cancer of the uterine cervix. Cancer Res 1996, 56:4509–4515.
9. Brizel DM, Scully SP, Harrelson JM, et al.: Tumor oxygenation predicts for the likelihood of distant metastases in human soft tissue sarcoma. Cancer Res 1996, 56:941–943.
10. Movsas B, Chapman JD, Horwitz EM, et al.: Hypoxic regions exist in human prostate carcinoma. Urology 1999, 53:11–18. This report represents the first study to obtain in vivo electrode measurements of oxygen levels in prostate cancer patients, and suggests that hypoxic regions exist in human prostate cancer. DOI: 10.1016/S0090-4295(98)00500-7
11. Movsas B, Chapman JD, Greenberg RE, et al.: Increasing levels of hypoxia in prostate carcinoma correlate significantly with increasing clinical stage and patient age: an Eppendorf pO(2) study. Cancer 2000, 89:2018–2024. DOI: 10.1002/1097-0142(20001101)89:9<2018::AID-CNCR19>3.3.CO;2-P
12. Cvetkovic D, Movsas B, Dicker AP, et al.: Increased hypoxia correlates with increased expression of the angiogenesis marker vascular endothelial growth factor in human prostate cancer. Urology 2001, 57:821–825. DOI: 10.1016/S0090-4295(00)01044-X
13. Movsas B, Chapman JD, Hanlon AL, et al.: Hypoxia in human prostate carcinoma: an Eppendorf PO2 study. Am J Clin Oncol 2001, 24:458–461. DOI: 10.1097/00000421-200110000-00009
14. Zhao D, Constantinescu A, Jiang L, et al.: Prognostic radiology: quantitative assessment of tumor oxygen dynamics by MRI. Am J Clin Oncol 2001, 24:462–466. DOI: 10.1097/00000421-200110000-00010
15. Shabsigh A, Tanji N, D’Agati V, et al.: Early effects of castration on the vascular system of the rat ventral prostate gland. Endocrinol 1999, 140:1920–1926. DOI: 10.1210/en.140.4.1920
16. Jain RK, Safabakhsh N, Sckell A, et al.: Endothelial cell death, angiogenesis, and microvascular function after castration in an androgen-dependent tumor: role of vascular endothelial growth factor. Proc Natl Acad Sci USA 1998, 95:10820–10825. DOI: 10.1073/pnas.95.18.10820
17. Semenza GL: HIF-1, O2, and the 3 PHDs: how animal cells signal hypoxia to the nucleus. Cell 2001, 107:1–3. DOI: 10.1016/S0092-8674(01)00518-9
18. Wang GL, Jiang B-H, Rue EA, Semenza GL: Hypoxia-inducible factor 1 is a basic-helix-loop-helix-PAS heterodimer regulated by cellular O2 tension. Proc Natl Acad Sci U S A 1995, 92:5510–5514. DOI: 10.1073/pnas.92.12.5510
19. Garayoa M, Martinez A, Lee S, et al.: Hypoxia-inducible factor-1 (HIF-1) up-regulates adrenomedullin expression in human tumor cell lines during oxygen deprivation: a possible promotion mechanism of carcinogenesis. Mol Endocrinol 2000, 14:848–862. DOI: 10.1210/me.14.6.848
20. Wang GL, Semenza GL: Purification and characterization of hypoxia-inducible factor 1. J Biol Chem 1995, 270:1230–1237. DOI: 10.1074/jbc.270.3.1230
21. Huang LE, Gu J, Schau B, Bunn HF: Regulation of hypoxiainducible factor 1-a is mediated by an O2-dependent degradation domain via the ubiquitin-proteasome pathway. Proc Natl Acad Sci U S A 1998, 95:7987–7992. DOI: 10.1073/pnas.95.14.7987
22. Maxwell PH, Wiesener MS, Chang GW, et al.: The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis. Nature 1999, 399:271–275. DOI: 10.1038/20459
23. Ivan M, Kondo K, Yang H, et al.: HIF a targeted for VHLmediated destruction by proline hydroxylation: implications for O2 sensing. Science 2001, 292:464–468. Report demonstrating that human pVHL binds to a short HIF-derived peptide when a conserved proline residue at the core of this peptide is hydroxylated. This protein modification may play a key role in mammalian oxygen sensing, because it requires molecular oxygen and Fe2+. DOI: 10.1126/science.1059817
24. Jaakkola P, Mole DR, Tian YM, et al.: Targeting of HIF-a to the von Hippel-Lindau ubiquitylation complex by O-regulated prolyl hydroxylation. Science 2001, 292:468–472. DOI: 10.1126/science.1059796
25. Zhong H, Chiles K, Feldser D, et al.: Modulation of hypoxiainducible factor 1α expression by the epidermal growth factor/phosphatidylinositol 3-kinase/PTEN/AKT/FRAP pathway in human prostate cancer cells: implications for tumor angiogenesis and therapeutics. Cancer Res 2000, 60:1541–1545. Important study reporting that pharmacologic agents that target PI-3K, AKT, or FRAP in tumor cells inhibit HIF-1α expression and may therefore be used as potential therapeutics.
26. Zundel W, Schindler C, Haas-Kogan D, et al.: Loss of PTEN facilitates HIF-1-mediated gene expression. Genes Dev 2000, 14:391–396.
27. Zhong H, Agani F, Baccala AA, et al.: Increased expression of hypoxia inducible factor-1a in rat and human prostate cancer. Cancer Res 1998, 58:5280–5284. In this report, expression of HIF-1α was evaluated in rat and human prostate cancer cell lines. It provided first evidence that HIF-1α may become dysregulated in prostate cancer, and that human cancer cells (PC-3 cells) can express HIF-1α protein under normoxic conditions.
28. Nupponen NN, Hyytinen ER, Kallioniemi AH, Visakorpi T: Genetic alterations in prostate cancer cell lines detected by comparative genomic hybridization. Cancer Genet Cytogenet 1998, 101:53–57. DOI: 10.1016/S0165-4608(97)00060-5
29. Saramäki OR, Savinainen KJ, Nupponen NN, et al.: Amplification of hypoxia-inducible factor 1a gene in prostate cancer. Cancer Genet Cytogenet 2001, 128:31–34. Short communication paper describing the amplification of the HIF-1α gene in the PC-3 cell line, which expresses the gene even under normoxic conditions. DOI: 10.1016/S0165-4608(01)00396-X
30. Zhong H, De Marzo M, Laughner E, et al.: Overexpression of hypoxia-inducible factor 1 a in common human cancers and their metastases. Cancer Res 1999, 59:5830–5935. Immunohistochemical study demonstrating that HIF-1α is overexpressed in the majority of prostate cancers (and other solid tumors), but is not detectable in benign prostatic tissues.
31. Talks KL, Turley H, Gatter KC, et al.: The expression and distribution of the hypoxia-inducible factors HIF-1a and HIF-2a in normal human tissues, cancers, and tumor-associated macrophages. Am J Pathol 2000, 157:411–421.
32. Salnikow K, Costa M, Figg WD, Blagosklonny MV: Hyperinducibility of hypoxia-responsive genes without p53/p21-dependent checkpoint in aggressive prostate cancer. Cancer Res 2000, 60:5630–5634.
33. Huss WJ, Hanrahan CF, Barrios RJ, et al.: Angiogenesis and prostate cancer: identification of a molecular progression switch. Cancer Res 2001, 61:2736–2743.
34. Aoki M, Schetter C, Himly M, et al.: The catalytic subunit of phosphoinositide 3-kinase: requirements for oncogenicity. J Biol Chem 2000, 275:6267–6275. DOI: 10.1074/jbc.275.9.6267
35. Jiang BH, Jiang G, Zheng JZ, et al.: Phosphatidylinositol 3-kinase signaling controls levels of hypoxia-inducible factor 1. Cell Growth Differ 2001, 12:363–369.
36. Toker A, Newton AC: Cellular signaling: pivoting around PDK-1. Cell 2000, 103:185–188. DOI: 10.1016/S0092-8674(00)00110-0
37. Cantley LC, Neel BG: New insight into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway. Proc Natl Acad Sci U S A 1999, 96:4240–4245. DOI: 10.1073/pnas.96.8.4240
38. McMenammin ME, Soung P, Perera S, et al.: Loss of PTEN expression in paraffin-embedded primary prostate cancer correlates with high Gleason score and advanced stage. Cancer Res 1999, 59:4291–4296.
39. Beitner-Johnson D, Rust RT, Hsieh TC, Millhorn DE: Hypoxia activates Akt and induces phosphorylation of GSK-3 in PC12 cells. Cell Signal 2001, 13:23–27. DOI: 10.1016/S0898-6568(00)00128-5
40. Chen EY, Mazure NM, Cooper JA, Giaccia AJ: Hypoxia activates a platelet-derived growth factor receptor/phosphatidylinositol 3-kinase/Akt pathway that results in glycogen synthase kinase-3 inactivation. Cancer Res 2001, 61:2429–2433.