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2012 | 10 | 3 | 236-243
Article title

Wybrane czynniki molekularne związane z przerzutowaniem raka jajnika

Content
Title variants
EN
Selected molecular factors associated with metastases of ovarian cancer
Languages of publication
EN
Abstracts
EN
Development of metastases is a typical feature of cancer progression and the main cause of treatment failure in cancer treatment. Due to their ability to settle far from original tumor location, cancer cells may preserve the feature of immortal cells, enabling survival of tumor and transition to chronic phase of the disease. Applying currently available techniques of topical treatment, such as surgery and radiotherapy, we are unable to control fully spread of cancer cells, while systemic chemotherapy even in chemosensitive tumors does not eradicate the disease in all cases. Ovarian cancer may spread by dissemination within the abdominal cavity and lymphatic vessels, resulting in distant metastases. The process of metastases’ development is extremely complex, depending on many different factors governing intercellular adhesion and acquisition of ability to move and migrate by cancer cells. Tumors with coexisting distant metastases are considered most advanced, which means also a grim prognosis for the patient. Mechanism of metastases’ development is the subject of several studies, attempting to identify factors which might lendthemselves for targeted therapy of cancers, including ovarian cancer. The paper presents genes, their products and other metastases-associated proteins: HER2 gene, AEG-1 gene, kisspeptin, E-cadherin, survivin, uPAR, clusterin, Met gene, claudins 3 and 4, kallikreins, SDF-1 gene. This paper is meant to systematize extensive knowledge on the development of metastases development and synthetic analysis of data concerning this process.
PL
Przerzutowanie jest cechą charakterystyczną progresji nowotworów złośliwych i główną przyczyną niepowodzeń w leczeniu raka. Dzięki zdolności do występowania w miejscach poza ogniskiem pierwotnym komórki nowotworowe mogą zachować cechę komórek nieśmiertelnych, co pozwala na przetrwanie nowotworu i nazwanie go chorobą przewlekłą. Stosując dostępne dziś metody leczenia miejscowego, takie jak chirurgia i radioterapia, nie jesteśmy w stanie w pełni kontrolować rozprzestrzeniania się komórek nowotworowych, a systemowa chemioterapia w chemiowrażliwych nowotworach nie zawsze „eradykuje” chorobę. Rak jajnika może szerzyć się poprzez rozsiew w jamie brzusznej oraz naczynia chłonne, dając przerzuty odległe. Proces przerzutowania jest niezmiernie złożony, wpływa na niego wiele różnych czynników decydujących o wzajemnym przyleganiu komórek do siebie, nabyciu zdolności ruchliwości i migracji przez komórki nowotworowe. Nowotwory, którym towarzyszą przerzuty odległe, są klasyfikowane jako najbardziej zaawansowane, co oznacza jednocześnie złe rokowanie dla pacjenta. Mechanizm przerzutowania jest przedmiotem wielu badań mających na celu wyłonienie czynników, które mogą być tarczą dla terapii celowanych nowotworów, w tym raka jajnika. W artykule przedstawiono geny i ich produkty oraz inne białka związane z przerzutowaniem: gen HER2, gen AEG-1, kisspeptynę, kadherynę-E, surwiwinę, uPAR, klusterynę, gen Met, klaudyny 3 i 4, kalikreiny, gen SDF-1. Celem pracy było usystematyzowanie obszernej wiedzy na temat przerzutowania oraz syntetyczna analiza danych dotyczących tego procesu.
Discipline
Publisher

Year
Volume
10
Issue
3
Pages
236-243
Physical description
Contributors
  • Klinika Perinatologii i Chorób Kobiecych, Uniwersytet Medyczny w Poznaniu. Kierownik: prof. dr hab. n. med. Krzysztof Drews
author
  • Katedra Onkologii, Uniwersytet Medyczny w Poznaniu. Kierownik: prof. dr hab. n. med. Janina Markowska
  • Katedra Onkologii, Uniwersytet Medyczny w Poznaniu. Kierownik: prof. dr hab. n. med. Janina Markowska
  • Katedra Onkologii, Uniwersytet Medyczny w Poznaniu. Kierownik: prof. dr hab. n. med. Janina Markowska
References
  • 1. Arteaga C.L.: Overview of epidermal growth factor receptor biology and its role as a therapeutic target in human neoplasia. Semin. Oncol. 2002; 29 (supl. 14): 3-9.
  • 2. Chuang T.C., Hsu S.C., Cheng Y.T. i wsp.: Magnolol downregulates HER2 gene expression, leading to inhibition of HER2-mediated metastatic potential in ovarian cancer cells. Cancer Lett. 2011; 311: 11-19.
  • 3. Bookman M.A., Darcy K.M., Clarke-Pearson D. i wsp.: Evaluation of monoclonal humanized anti-HER2 antibody, trastuzumab, in patients with recurrent or refractory ovarian or primary peritoneal carcinoma with overexpression of HER2: a phase II trial of the Gynecologic Oncology Group. J. Clin. Oncol. 2003; 21: 283-290.
  • 4. Sheng Q., Liu J.: The therapeutic potential of targeting the EGFR family in epithelial ovarian cancer. Br. J. Cancer 2011; 104: 1241-1245.
  • 5. Yoo B.K., Emdad L., Lee S.G. i wsp.: Astrocyte elevated gene-1 (AEG-1): a multifunctional regulator of normal and abnormal physiology. Pharmacol. Ther. 2011; 130: 1-8.
  • 6. Lee S.G., Su Z.Z., Emdad L. i wsp.: Astrocyte elevated gene-1 (AEG-1) is a target gene of oncogenic Ha-ras requiring phosphatidylinositol 3-kinase and c-Myc. Proc. Natl Acad. Sci. USA 2006; 103: 17390-17395.
  • 7. Emdad L., Sarkar D., Su Z.Z. i wsp.: Activation of the nuclear factor κB pathway by astrocyte elevated gene-1: implications for tumor progression and metastasis. Cancer Res. 2006; 66: 1509-1516.
  • 8. Li C., Liu J., Lu R. i wsp.: AEG-1 overexpression: a novel indicator for peritoneal dissemination and lymph node metastasis in epithelial ovarian cancers. Int. J. Gynecol. Cancer 2011; 21: 602-608.
  • 9. Meng F., Luo C., Ma L. i wsp.: Clinical significance of astrocyte elevated gene-1 expression in human epithelial ovarian carcinoma. Int. J. Gynecol. Pathol. 2011; 30: 145-150.
  • 10. Emdad L., Sarkar D., Lee S.G. i wsp.: Astrocyte elevated gene-1: a novel target for human glioma therapy. Mol. Cancer Ther. 2010; 9: 79-88.
  • 11. Roa J., Tena-Sempere M.: KiSS-1 system and reproduction: comparative aspects and roles in the control of female gonadotropic axis in mammals. Gen. Comp. Edocrinol. 2007; 153: 132-140.
  • 12. Makri A., Pissimissis N., Lembessis P. i wsp.: The kisspeptin (KiSS-1)/GPR54 system in cancer biology. Cancer Treat. Rev. 2008; 34: 682-692.
  • 13. Prentice L.M., Klausen C., Kalloger S. i wsp.: Kisspeptin and GPR54 immunoreactivity in a cohort of 518 patients defines favourable prognosis and clear cell subtype in ovarian carcinoma. BMC Med. 2007; 5: 33.
  • 14. Hata K., Dhar D.K., Watanabe Y. i wsp.: Expression of metastin and a G-protein-coupled receptor (AXOR12) in epithelial ovarian cancer. Eur. J. Cancer 2007; 43: 1452-1459.
  • 15. Jiang Y., Berk M., Singh L.S. i wsp.: KiSS1 suppresses metastasis in human ovarian cancer via inhibition of protein kinase C alpha. Clin. Exp. Metastasis 2005; 22: 369-376.
  • 16. Hajra K.M., Fearon E.R.: Cadherin and catenin alterations in human cancer. Gene Chromosomes Cancer 2002; 34: 255-268.
  • 17. Auersperg N., Wong A.S., Choi K. i wsp.: Ovarian surface epithelium: biology, endocrinology, and pathology. Endocr. Rev. 2001; 22: 255-288.
  • 18. Elloul S., Silins I., Trope C.G. i wsp.: Expression of E-cadherin transcriptional regulators in ovarian carcinoma. Virchows Arch. 2006; 449: 520-528.
  • 19. Sawada K., Mitra A.K., Radjabi A.R. i wsp.: Loss of E-cadherin promotes ovarian cancer metastasis via α5-integrin, which is a therapeutic target. Cancer Res. 2008; 68: 2329-2339.
  • 20. Ho C.M., Cheng W.F., Lin M.C. i wsp.: Prognostic and predictive values of E-cadherin for patients of ovarian clear cell adenocarcinoma. Int. J. Gynecol. Cancer 2010; 20: 1490-1497.
  • 21. Urbaniak J.: Expression of survivin in human cancer. Adv. Clin. Exp. Med. 2004; 13: 1037-1046.
  • 22. Liguang Z., Peishu L., Hongluan M. i wsp.: Survivin expression in ovarian cancer. Exp. Oncol. 2007; 29: 121-125.
  • 23. No J.H., Jeon Y.T., Kim Y.B., Song Y.S.: Quantitative detection of serum survivin and its relationship with prognostic factors in ovarian cancer. Gynecol. Obstet. Invest. 2011; 71: 136-140.
  • 24. Smith H.W., Marshall C.J.: Regulation of cell signalling by uPAR. Nat. Rev. Mol. Cell Biol. 2010; 11: 23-36.
  • 25. Wei Y., Tang C.H., Kim Y. i wsp.: Urokinase receptors are required for α5β1 integrin-mediated signaling in tumor cells. J. Biol. Chem. 2007; 282: 3929-3939.
  • 26. Wang L., Madigan M.C., Chen H. i wsp.: Expression of urokinase plasminogen activator and its receptor in advanced epithelial ovarian cancer patients. Gynecol. Oncol. 2009; 114: 265-267.
  • 27. Kenny H.A., Leonhardt P., Ladanyi A. i wsp.: Targeting the urokinase plasminogen activator receptor inhibits ovarian cancer metastasis. Clin. Cancer Res. 2011; 17: 459-471.
  • 28. Shannan B., Seifert M., Leskov K. i wsp.: Challenge and promise: roles for clusterin in pathogenesis, progression and therapy of cancer. Cell Death Differ. 2006; 13: 12-19.
  • 29. Yang G.F., Li X.M., Xie D.: Overexpression of clusterin in ovarian cancer is correlated with impaired survival. Int. J. Gynecol. Cancer 2009; 19: 1342-1346.
  • 30. Hassan M.K., Watari M., Christenson L. i wsp.: Intracellular clusterin negatively regulates ovarian chemoresistance: compromised expression sensitizes ovarian cancer cells to paclitaxel. Tumour Biol. 2011; 32: 1031-1047.
  • 31. Wei L., Xue T., Wang J. i wsp.: Roles of clusterin in progression, chemoresistance and metastasis of human ovarian cancer. Int. J. Cancer 2009; 125: 791-806.
  • 32. Park D.C., Yeo S.G., Wilson M.R. i wsp.: Clusterin interacts with paclitaxel and confer paclitaxel resistance in ovarian cancer. Neoplasia 2008; 10: 964-972.
  • 33. Zhou H.Y., Pon Y.L., Wong A.S.: HGF/MET signaling in ovarian cancer. Curr. Mol. Med. 2008; 8: 469-480.
  • 34. Mitra A.K., Sawada K., Tiwari P. i wsp.: Ligand independent activation of c-Met by fibronectin and α5β1-integrin regulates ovarian cancer invasion and metastasis. Oncogene 2011; 30: 1566-1576.
  • 35. Sourbier C.: Met and the microenvironment: new insights for ovarian cancer metastasis. Cell Adh. Migr. 2011; 5: 209-210.
  • 36. Ayhan A., Ertunc D., Tok E.C., Ayhan A.: Expression of the c-Met in advanced epithelial ovarian cancer and its prognostic significance. Int. J. Gynecol. Cancer 2005; 15: 618-623.
  • 37. Martin T.A., Jiang W.G.: Loss of tight junction barrier function and its role in cancer metastasis. Biochim. Biophys. Acta 2009; 1788: 872-891.
  • 38. Agarwal R., D’Souza T., Morin P.J.: Claudin-3 and claudin-4 expression in ovarian epithelial cells enhances invasion and is associated with increased matrix metalloproteinase-2 activity. Cancer Res. 2005; 65: 7378-7385.
  • 39. Shih I.M., Davidson B.: Pathogenesis of ovarian cancer: clues from selected overexpressed genes. Future Oncol. 2009; 5: 1641.
  • 40. Yousef G.M., Diamandis E.P.: The new human tissue kallikrein gene family: structure, function, and association to disease. Endocr. Rev. 2001; 22: 184-204.
  • 41. Ghosh M.C., Grass L., Soosaipillai A. i wsp.: Human kallikrein 6 degrades extracellular matrix proteins and may enhance the metastatic potential of tumour cells. Tumour Biol. 2004; 25: 193-199.
  • 42. Dorn J., Harbeck N., Kates R. i wsp.: Impact of expression differences of kallikrein-related peptidases and of uPA and PAI-1 between primary tumor and omentum metastasis in advanced ovarian cancer. Ann. Oncol. 2011; 22: 877-883.
  • 43. Kucia M., Jankowski K., Reca R. i wsp.: CXCR4-SDF-1 signalling, locomotion, chemotaxis and adhesion. J. Mol. Histol. 2004; 35: 233-245.
  • 44. Hall J.M., Korach K.S.: Stromal cell-derived factor 1, a novel target of estrogen receptor action, mediates the mitogenic effects of estradiol in ovarian and breast cancer cells. Mol. Endocrinol. 2003; 17: 792-803.
  • 45. Maksym R.B., Tarnowski M., Grymula K. i wsp.: The role of stromal-derived factor-1 – CXCR7 axis in development and cancer. Eur. J. Pharmacol. 2009; 625: 31-40.
  • 46. Hawkins O.E., Richmond A.: The dynamic yin-yang interaction of CXCR4 and CXCR7 in breast cancer metastasis. Breast Cancer Res. 2012; 14: 103.
Document Type
article
Publication order reference
Identifiers
YADDA identifier
bwmeta1.element.psjd-8b95dcb3-5453-47bd-9fc3-e8d1f43d2c74
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