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Original Research

Open Access

Nuclear factor-kappa beta pathway and endometrial cancer: a pilot study

  • E. Yilmaz1,*,
  • E.I. Coskun1
  • M. Gul2
  • N. Sahin3
  • G. Tuncay1
  • Y. Simsek4

1Department of Obstetrics and Gynecology, Kırıkkale (Turkey)

2Department of Histology and Embryology,Kırıkkale (Turkey)

3Department of Pathology, Inonu University School of Medicine, Malatya

4 Private Clinic, Kırıkkale (Turkey)

DOI: 10.12892/ejgo3471.2017 Vol.38,Issue 4,August 2017 pp.536-540

Published: 10 August 2017

*Corresponding Author(s): E. Yilmaz E-mail: ercanyilmazgyn@yahoo.com

Abstract

Objective: Examination of the role of nuclear factor-kappa beta (NF-kB) expression in the etiopathogenesis of endometrial cancer, by means of the immunohistochemical method. Materials and Methods: Patients who applied to participate in the study at the clinic were grouped into three categories: those diagnosed with benign endometrial pathology, those with endometrial hyperplasia, and those with endometrial cancer. NF-kB analysis was conducted in the endometrial tissues of the patients’ paraffin blocks by means of the immunohistochemical method. For objective assessment purposes, the H score of each patient was calculated. SPSS 15.0 program was employed for statistical analysis. Results: The average H score of the first group, comprising benign endometrial pathologies, was 102.4 ± 85.9, that of the hyperplasia group was 143.6 ± 122.4, and that of the cancer group was 276.8 ± 61.8. The average values of groups 1 and 2 were similar (p = 0.349); however, the third group’s average H score was significantly higher (p < 0.001). Conclusion: NF-kB, which is a critical mediator in the inflammation process, might be related to the development of premalign and malign endometrial changes.

Keywords

Endometrial cancer; Endometrial hyperplasia; Inflammation; NF-kB.

Cite and Share

E. Yilmaz,E.I. Coskun,M. Gul,N. Sahin,G. Tuncay,Y. Simsek. Nuclear factor-kappa beta pathway and endometrial cancer: a pilot study. European Journal of Gynaecological Oncology. 2017. 38(4);536-540.

References

[1] Elit L.M., Pond G., Seow H.: “Time interval between endometrial biopsy and surgical staging for type I endometrial cancer: association between tumor characteristics and survival outcome”. Obstet. Gynecol., 2015, 125, 1497.

[2] Kwon J.S.: “Improving survival after endometrial cancer: the big picture”. J. Gynecol. Oncol., 2015, 26, 227.

[3] Kim M.K., Seong S.J., Kim J.W., Bae D.S., Jeon S., Kwon S.H., Lee T.S.: “Management of endometrial hyperplasia: a survey of members of the Korean Gynecologic Oncology Group”. Int. J. Gynecol. Cancer, 2015, 25, 1277.

[4] Daud S., Jalil S.S., Griffin M., Ewies A.A.: “Endometrial hyperplasia - the dilemma of management remains: a retrospective observational study of 280 women”. Eur. J. Obstet. Gynecol. Reprod. Biol., 2011, 159, 172.

[5] Aggarwal B.B., Shishodia S., Sandur S.K., Pandey M.K., Sethi G.: “Inflammation and cancer: how hot is the link?” Biochem. Pharmacol., 2006, 30, 1605.

[6] Walton C.B., Matter M.L.: “Chromatin immunoprecipitation assay: examining the interaction of NFkB with the VEGF promoter”. Methods Mol. Biol., 2015, 1332, 75.

[7] Simsek Y., Gul M., Celik O., Aydin N.E., Arda Düz S., Celik E., et al.: “Nuclear transcription factor-kappa beta-dependent ultrastructural alterations within the placenta and systemic inflammatory activation in pregnant patients with hemolysis, elevated liver functions and low thrombocyte count (HELLP) syndrome: a case-control study”. Hypertens. Pregnancy, 2013, 32, 281.

[8] Budwit-Novotny D.A., McCarty K.S., Cox E.B., Soper J.T., Mutch D.G., Creasman W.T., et al.: “Immunohistochemical analyses of estrogen receptor in endometrial adenocarcinoma using a monoclonal antibody”. Cancer Res., 1986, 46, 5419.

[9] Talhouk A., McConechy M.K., Leung S., Li-Chang H.H., Kwon J.S., Melnyk N., et al.: “A clinically applicable molecular-based classification for endometrial cancers. Br J Cancer 2015; 113: 299.

[10] Kamp D.W., Shacter E., Weitzman S.A.: “Chronic inflammation and cancer: the role of the mitochondria”. Oncology, 2011, 25, 400.

[11] Ramos-Nino M.E.: “The role of chronic inflammation in obesity-associated cancers”. ISRN Oncol., 2013, 2013, 697521

[12] Vendramini-Costa D.B, Carvalho J.E.: “Molecular link mechanisms between inflammation and cancer”. Curr. Pharm. Des., 2012, 18, 3831.

[13] Koehne C.H., Dubois R.N.: “COX-2 inhibition and colorectal cancer”. Semin. Oncol., 2004, 31, 12.

[14] Shebl F.M., Sakoda L.C., Black A., Koshiol J., Andriole G.L., Grubb R., et al.: “Aspirin but not ibuprofen use is associated with reduced risk of prostate cancer: a PLCO study”. Br. J. Cancer, 2012, 107, 207.

[15] Arango H.A., Icely S., Roberts W.S., Cavanagh D., Becker J.L.: “Aspirin effects on endometrial cancer cell growth”. Obstet. Gynecol., 2001, 97, 423.

[16] Dossus L., Rinaldi S., Becker S., Lukanova A., Tjonneland A., Olsen A., et al.: “Obesity, inflammatory markers, and endometrial cancer risk: a prospective case-control study”. Endocr. Relat. Cancer, 2010, 17, 1007.

[17] Chen C.D., Sawyers C.L.: “NF-kappa B activates prostate-specific antigen expression and is upregulated in androgen-independent prostate cancer”. Mol. Cell Biol., 2002, 22, 2862

[18] Karin M., Cao Y., Greten F.R., Li Z.W.: “NF-kappaB in cancer: from innocent bystander to major culprit”. Nat. Rev. Cancer, 2002, 2, 301.

[19] Chen Y., Lu R., Zheng H., Xiao R., Feng J., Wang H., Gao X., Guo L.: “The NFKB1 polymorphism (rs4648068) is associated with the cell proliferation and motility in gastric cancer”. BMC Gastroenterol., 2015, 14, 1.

[20] Mosialos G.: “The role of Rel/NF-kappa B proteins in viral oncogenesis and the regulation of viral transcription”. Semin. Cancer Biol., 1997, 8, 121.

[21] Dolcet X., Llobet D., Pallares J., Matias-Guiu X.: “NF-kB in development and progression of human cancer”. Virchows Arch., 2005, 446, 475.

[22] Nagel S., Ehrentraut S., Meyer C., Kaufmann M., Drexler H.G., MacLeod R.A.: “NFkB is activated by multiple mechanisms in hairy cell leukemia”. Genes Chromosomes Cancer, 2015, 54, 418.

[23] Khan S., Lopez-Dee Z., Kumar R., Ling J.: “Activation of NFkB is a novel mechanism of pro-survival activity of glucocorticoids in breast cancer cells”. Cancer Lett., 2013, 337, 90.

[24] Lundqvist J., Yde C.W., Lykkesfeldt A.E.: “1α,25-dihydroxyvitamin D3 inhibits cell growth and NFºB signaling in tamoxifenresistant breast cancer cells”. Steroids, 2014, 85, 30.

[25] Moorchung N., Kunwar S., Ahmed K.W.: “An evaluation of nuclear factor kappa B expression in colorectal carcinoma: an analysis of 50 cases”. J. Cancer Res. Ther., 2014, 10, 631.

[26] Akca H., Demiray A., Tokgun O., Yokota J.: “Invasiveness and anchorage independent growth ability augmented by PTEN inactivation through the PI3K / AKT / NFkB pathway in lung cancer cells”. Lung Cancer, 2011, 73, 302.

[27] Hu J., Meng Y., Yu T., Hu L., Mao M.: “Ubiquitin E3 ligase MARCH7 promotes ovarian tumor growth”. Oncotarget, 2015, 6, 12174.

[28] Lisanti M.P., Martinez-Outschoorn U.E., Sotgia F.: “Oncogenes induce the cancer-associated fibroblast phenotype: metabolic symbiosis and “fibroblast addiction” are new therapeutic targets for drug discovery”. Cell Cycle, 2013, 12, 2723.

[29] Barlin J.N., Jelinic P., Olvera N., Bogomolniy F., Bisogna M., Dao F., et al.: “Validated gene targets associated with curatively treated advanced serous ovarian carcinoma”. Gynecol. Oncol., 2013, 128, 512.

[30] Divya C.S., Pillai M.R.: “Antitumor action of curcumin in human papillomavirus associated cells involves downregulation of viral oncogenes, prevention of NFkB and AP-1 translocation, and modulation of apoptosis”. Mol. Carcinog., 2006, 45, 320.

[31] St-Germain M.E., Gagnon V., Parent S., Asselin E.: “Regulation of COX-2 protein expression by Akt in endometrial cancer cells is mediated through NF-kappaB/IkappaB pathway”. Mol. Cancer, 2004, 3, 7.

[32] Vaskivuo T.E., Stenbäck F., Tapanainen J.S.: “Apoptosis and apoptosis-related factors Bcl-2, Bax, tumor necrosis factor-alpha, and NFkappaB in human endometrial hyperplasia and carcinoma”. Cancer, 2002, 95, 1463.

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