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Original Research

Open Access

Interleukin-17 promotes ovarian carcinoma SKOV3 cells via MTA1-induced epithelial-to-mesenchymal transition

  • N. Guo1,2
  • J. Zhang1,2,*,

1The Department of Obstetrics and Gynecology, West China Second University Hospital of Sichuan University, Chengdu, Sichuan

2Key laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education (China)

DOI: 10.31083/j.ejgo.2020.01.4933 Vol.41,Issue 1,February 2020 pp.70-74

Published: 15 February 2020

*Corresponding Author(s): J. Zhang E-mail:


Objectives: Interleukin-17 (IL-17) induced chronic inflammation has been associated with development, invasion, and metastasis of tumors, which has been demonstrated to promote development of ovarian cancer, prostate cancer, colon cancer, skin cancer, breast cancer, lung cancer and pancreatic cancer. The present authors found that IL-17 promoted ovarian cancer developed, in addition, with a concurrent increase of metastasis-associated genes-1 (MTA1). Whether IL-17 mediates MTA1’s action and the underlying mechanisms remain unknown. Material and Methods: Cell invasion was detected by wound-healing assay and transwell assay after treatment with IL-17 at 20 ng/ml concentrations for 24 hours. The apoptotic rates of cells were detected by a flow cytometer (FCM) after IL-17 treatment at 20 ng/ml concentrations for 24 hours. The expression of MTA1, Vimentin, Twist, Snail, Slug, N-cadherin, and E-cadherin was detected by Western blot analysis and reverse transcription polymerase chain reaction (RT-PCR) after treatment with 20 ng/ml of IL17 for 8, 16, 24, and 36 hours, respectively. Results: Wound-healing assay and transwell assay demonstrated IL-17 increases ovarian carcinoma cell invasion, and the FCM showed that the apoptotic rates in the IL-17 group were lower than those in the control group (p < 0.01). Western blot analysis detected that MTA1, Vimentin, Twist, Snail, slug, and N-cadherin in the IL-17 group were higher than those in the control group, E-cadherin in the IL-17 group were lower than those in the control group, and RT-PCR detected that MTA1 mRNA levels were positively correlated with the time of IL-17 affected on ovarian carcinoma cells (p < 0.05). Conclusions: IL-17 induces MTA1 expression to enhancing epithelial-to-mesenchymal transition (EMT) and tumor cell invasion, which indicates IL-17- MTA1-EMT axis as potential targets for developing new strategies in the prevention and treatment of ovarian cancer.


IL-17; MTA1; Epithelial-to-mesenchymal transition; Ovarian cancer

Cite and Share

N. Guo,J. Zhang. Interleukin-17 promotes ovarian carcinoma SKOV3 cells via MTA1-induced epithelial-to-mesenchymal transition. European Journal of Gynaecological Oncology. 2020. 41(1);70-74.


[1] Lim H.J., Ledger W.: “Targeted therapy in ovarian cancer”. Womens Health (Lond.), 2016, 12, 363.

[2] Guo N., Peng Z., Zhang J: “Proteasome inhibitor MG132 enhances sensitivity to cisplatin in ovarian carcinoma cells in vitro and in vivo”. Int. J. Gynecol. Cancer, 2016, 26, 839.

[3] Zhang Q1, Liu S1, Parajuli KR1, Zhang W2, Zhang K2, Mo Z., et al.: “Interleukin-17 promotes prostate cancer via MMP-7induced cpithelial-to-mesenchumal transition”. Oncogene, 2017, 36, 687.

[4] Onishi R.M., Gaffen S.L.: “Interleukin-17 and its target genes: mechanisms of interleukin-17 function in disease”. Immunology, 2010. 129, 311.

[5] McAleer J.P., Kolls J.K.: “Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense”. Immunol. Rev., 2014, 260, 129.

[6] Winkler I., Pyszniak M., Pogoda K., Semczuk A., Gogacz M., Miotla P, Adamiak A., et al.: “Assessment of Th17 lymphocytes and cytokine IL-17A in epithelial ovarian tumors”. Oncol. Rep., 2017, 37, 3107.

[7] Zhang Q., Liu S., Ge D., Zhang Q., Xue Y., Xiong Z., et al.: “Interleukin-17 promotes formation and growth of prostate adenocarcinoma in mouse models”. Cancer Res., 2012, 72, 2589.

[8] Wu S., Rhee K.J., Albesiano E., Rabizadeh S., Wu X., Yen H.R., et al.: “A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responses”. Nat. Med., 2009, 15, 1016.

[9] Xiao M., Wang C., Zhang J., Li Z., Zhao X., Qin Z.: “IFNgamma promotes papilloma development by up-regulating Th17-associated inflammation”. Cancer Res., 2009, 69, 2010.

[10] Novitskiy S.V., Pickup M.W., Gorska A.E., Owens P., Chytil A., Aakre M., et al.: “TGF-β receptor II loss promotes mammary carcinoma progression by Th17 dependent mechanisms”. Cancer Discov., 2011, 1, 430.

[11] Xu B., Guenther J.F., Pociask D.A., Wang Y., Kolls J.K., You Z., et al.: “Promotion of lung tumor growth by interleukin-17”. Am. J. Physiol. Lung Cell Mol. Physiol., 2014, 307, L497.

[12] McAllister F., Bailey J.M., Alsina J., Nirschl C.J., Sharma R., Fan H., et al.: “Oncogenic Kras activates a hematopoietic-to-epithelial IL-17 signaling axis in preinvasive pancreatic neoplasia”. Cancer Cell, 2014, 25, 621.

[13] Sen N., Gui B., Kumar R.: “Role of MTA1 in cancer progression and metastasis”. Cancer Metastasis Rev., 2014, 33, 879.

[14] Dhasarathy A., Kajita M., Wade P.A.: “The transcription factor snail mediates epithelial to mesenchymal transitions by repression of estrogen receptor-alpha”. Mol. Endocrinol., 2007, 21, 2907.

[15] Weng W., Yin J., Zhang Y., Qiu J., Wang X.: “Metastasis-associated protein 1 promotes tumor invasion by downregulation of E-cadherin’. Int. J. Oncol., 2014, 44, 812.

[16] Kumar R.: “Another tie that binds the MTA family to breast cancer”. Cell, 2003, 113, 142.

[17] Song Y., Yang J.M.: “Role of interleukin (IL)-17 and T-helper (Th)17 cells in cancer”. Biochem. Biophys. Res. Commun., 2017, 493, 1.

[18] Toh Y., Nicolson G.L.: “Properties and clinical relevance of MTA1 protein in human cancer”. Cancer Metastasis Rev., 2014, 33, 891.

[19] Hanahan D., Weinberg R.A.: “The hallmarks of cancer”. Cell, 2000, 100, 57.

[20] Zou W., Restifo N.P.: “T(H)17 cells in tumour immunity and immunotherapy”. Nat. Rev. Immunol., 2010, 10, 248.

[21] Numasaki M., Fukushi J., Ono M., Narula S.K., Zavodny P.J., Kudo T., et al.: “Interleukin-17 promotes angiogenesis and tumor growth. Blood, 2003, 101, 2620.

[22] Hirahara N., Nio Y., Sasaki S., Minari Y., Takamura M., Iguchi C., et al.: “Inoculation of human interleukin-17 gene-transfected Meth-A fibrosarcoma cells induces T cell-dependent tumor-specific immunity in mice’. Oncology, 2001, 61, 79.

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