Hypoxia - an explanation of prostate cancer progression mechanisms

  • Paweł Szymański Department of Radiotherapy the F. Lukaszczyk Oncology Centre, Bydgoszcz 85-796, Romanowskiej 2, Poland
  • Krzysztof Roszkowski Department of Oncology, Radiotherapy and Gynecologic Oncology, Collegium Medicum, Nicolaus Copernicus University, Bydgoszcz 85-796, Romanowskiej 2, Poland
Keywords: Hypoxia, Prostate cancer, Cancer stem cells

Abstract

Prostate cancer (PC) is a common malignancy in males in most industrialized countries, where it is the most commonly diagnosed cancer affecting men after middle age (>50 years). Although the screening and surgical procedures for prostate cancer have improved, successful treatment is still a major challenge. In the tumor microenvironment, hypoxia is one of the crucial factors which promote an aggressive phenotype of tumor cells and decrease the effectiveness of standard treatment. It implies that tumor cells surviving hypoxic stress are likely to be a significant source of viable clonogens that can repopulate tumors with more malignant/metastatic cells. Unfortunately, most treatment protocols are less effective against hypoxic cells which are resistant not only to radiotherapy, but also to standard cytotoxic chemotherapy. There is now a considerable amount of clinical evidence that tumors with a higher proportion of hypoxic cells have a poor diagnosis. Tolerance of hypoxic conditions varies in different tumor types. However, prostate cancer cells seem to be highly tolerant of hypoxia. The main problem concerning the effectiveness of prostate tumor therapies are changes in the biology of hypoxic tumor cells after standard hormone- and radiotherapy. Despite the many studies of tumor hypoxia, very little attention has been given to the oxygen concentration in the conditions of in vitro cancer cells studies. To date, there has been no comprehensive characterization of prostate cancer cells under hypoxic condition, which seems to be crucial in the light of the intensive search for novel cancer therapies.

DOI: http://dx.doi.org/10.5281/zenodo.2567558

References

1. Fioriti D, Mischitelli M, Di Monaco F, et al. Cancer stem cells in prostate adenocarcinoma: a target for new anticancer strategies. J Cell Physiol. 2008; 216: 571-575.

2. Sekhon K, Bucay N, Majid S, et al. MicroRNAs and epithelial-mesenchymal transition in prostate cancer. Oncotarget. 2016; 7: 67597-67611.

3. McKeown SR. Defining normoxia, physoxia and hypoxia in tumours – implications for treatment response. Br J Radiol. 2013; 87(1035): 20130676.

4. Mimeault M, Batra SK. Hypoxia-inducing factors as master regulators of stemness properties and altered metabolism of cancer- and metastasis-initiating cells. J Cell Mol Med. 2013; 17: 30-54.

5. Shah H, Vaishampayan U. Therapy of advanced prostate cancer: targeting the androgen receptor axis in earlier lines of treatment. Target Oncol. 2018; 13: 679-689.

6. Miao ZF, Zhao TT, Wang ZN, et al. Influence of different hypoxia models on metastatic potential of SGC-7901 gastric cancer cells. Tumor Biol. 2014; 35: 6801-6808.

7. Gezer D, Vykovic M, Soga T, et al. Concise review: genetic dissection of hypoxia signaling pathways in normal and leukemic stem cells. Stem Cells. 2014; 32: 1390-1397.

8. Gilany K, Vafakhah M. Hypoxia: a Review. J Paramed Sci. 2010; 1: 43-60.

9. Olbryt M, Habryka A, Student S, et al. Global gene expression profiling in three tumor cell lines subjected to experimental cycling and chronic hypoxia. Plos One. 2014; 9: e105104.

10. Bhaskara VK, Mohanam I, Rao JS, et al. Intermittent hypoxia regulates stem-like characteristics and differentiation of neuroblastoma cells. Plos One. 2012; 7: e30905.

11. Leao R, Domingos C, Figueiredo A, et al. Cancer stem cells in prostate cancer implications for targeted therapy. Urol Int. 2017; 99: 125-136.

12. Nguyen LV, Vanner R, Dirks P, et al. Cancer stem cells an evolving concept. Nat Rev. Cancer. 2012; 12: 133-143.

13. Kreso A, O'Brien CA, van Galen P, et al. Variable clonal repopulation dynamics influence chemotherapy response in colorectal cancer. Science. 2013; 339: 543-548.

14. Fessler E, Dijkgraaf FE, De Sousa E, et al. Cancer stem cell dynamics in tumor progression and metastasis: is the microenvironment to blame? Cancer Lett. 2013; 341: 97-104.

15. Glumac PM, LeBeau AM. The role of CD133 in cancer: a concise review. Clin Transl Med. 2018; 7: 18.

16. Kanwal R, Shukla S, Walker E, et al. Acquisition of tumorigenic potential and therapeutic resistance in CD133+ subpopulation of prostate cancer cells exhibiting stem-cell like characteristics. Cancer Lett. 2018; 430: 25-33.

17. Erdogan S, Doganlar ZB, Doganlar O, et al. Inhibition of midkine suppresses prostate cancer CD133+ stem cell growth and migration. Am J Med Sci. 2017; 354: 299-309.

18. Cojoc M, Mabert K, Muders MH, et al. A role for cancer stem cells in therapy resistance: cellular and molecular mechanisms. Semin Cancer Biol. 2015; 31:16-27.

19. Tang DG. Understanding cancer stem cell heterogeneity and plasticity. Cell Research. 2012; 22: 457-472.

20. Macklin PS, McAuliffe J, Pugh CW, et al. Hypoxia and HIF pathway in cancer and the placenta. Placenta. 2017; 56: 8-13.

21. Liu ZJ, Semenza GL, Zhang HF. Hypoxia-inducible factor 1 and breast cancer metastasis. J Zhejiang Univ Sci B. 2015; 16: 32-43.

22. Vadde R, Vemula S, Jinka R, et al. Role of hypoxia-inducible factors (HIF) in the maintenance of stemness and malignancy of colorectal cancer. Crit Rev Oncol Hematol. 2017; 113: 22-27.

23. Yao M, Rogers L, Suchowerska N, et al. Sensitization of prostate cancer to radiation therapy: molecules and pathways to target. Radiother Oncol. 2018; 128: 283-300.

24. Reyes EE, Gillard M, Duggan R, et al. Molecular analysis of CD133-positive circulating tumor cells from patients with metastatic castration-resistant prostate cancer. J Transl Sci. 2015; 1: 1-19.

25. Pastushenko I, Blanpain C. EMT transition states during tumor progression and metastasis. Trends Cell Biol. 2018; pii: S0962-8924(18)30201-0.

26. Santamaria PG, Moreno-Bueno G, Portillo F, et al. EMT: Present and future in clinical oncology. Mol Oncol. 2017; 11: 718-738.

27. Liang L, Sun H, Zhang W, et al. Meta-analysis of EMT datasets reveals different types of EMT. PLoS One. 2016; 11: e0156839.

28. Lamouille S, Xu J, Derynck R. Molecular mechanisms of epithelial-mesenchymal transition. Nat Rev Mol Cell Biol. 2014; 15: 178-196.

29. Jiang J, Tang Y, Liang X. EMT – a new vision of hypoxia promoting cancer progression. Cancer Biol Ther. 2011; 11: 714-723.

30. Huang L, Wu RL, Xu AM. Epithelial-mesenchymal transition in gastric cancer. Am J Transl Res. 2015; 7: 2141-2158.

31. Nantajit D, Lin D, Li JJ. The network of epithelial-mesenchymal transition: potential new targets for tumor resistance. J Cancer Res Clin Oncol. 2014; 141(10): 1697-1713.

32. Steinestel K, Eder S, Schrader AJ, et al. Clinical significance of epithelial-mesenchymal transition. Clin Transl Med. 2014; 3: 17.

33. Kim DH, Xing T, Yang Z, et al. Epithelial mesenchymal transition in embryonic development, tissue repair and cancer: a comprehensive overview. J Clin Med. 2018; 7: 1.

34. Xiong L, Wen Y, Miao X, et al. NT5E and FcGBP as key regulators of TGF-1-induced epithelial-mesenchymal transition (EMT) are associated with tumor progression and survival of patients with gallbladder cancer. Cell Tissue Res. 2014; 355: 365-374.

35. Figueiró F, Mendes FB, Corbelini PF, et al. A monastrol-derived compound, LaSOM 63, inhibits ecto-5'nucleotidase/CD73 activity and induces apoptotic cell death of glioma cell lines. Anticancer Res. 2014; 34: 1837-1842.

36. Eltzschig HK, Ibla JC, Furuta GT, et al. Coordinated adenine nucleotide phosphohydrolysis and nucleoside signaling in posthypoxic endothelium: Role of ectonucleotidases and adenosine A2B receptors. J Exp Med. 2003; 198: 783Y96.

37. Gessi S, Merighi S, Sacchetto V, et al. Adenosine receptors and cancer. Biochim Biophys Acta. 2011; 1808: 1400-1412.

38. Mifsud A, Choon AT, Fang D, et al. Prostate-specific antigen, testosterone, sex-hormone binding globulin and androgen receptor CAG repeat polymorphisms in subfertility and normal men. Mol Hum Reprod. 2001; 7: 1007-1013.

39. Giwercman A, Kledal T, Schwartz M, et al. Preserved male fertility despite decreased androgen sensitivity caused by a mutation in the ligand-binding domain of the androgen receptor gene. J Clin Endocrinol Metab. 2000; 85(6): 2253-2259.

40. Tan MH, Li J, Xu HE, et al. Androgen receptor: structure, role in prostate cancer and drug discovery. Acta Pharmacol Sin. 2015; 36(1): 3-23.

41. Marcelli M, Ittmann M, Mariani S, et al. Androgen receptor mutations in prostate cancer. Cancer Research. 2000; 60: 944-949.
Published
2019-02-07
How to Cite
Szymański, P., & Roszkowski, K. (2019). Hypoxia - an explanation of prostate cancer progression mechanisms. MicroMedicine, 7(1), 5-12. Retrieved from http://journals.tmkarpinski.com/index.php/mmed/article/view/142
Section
Review Articles