TGF-β1 and IL-10 expression in epithelial ovarian cancer cell line A2780
Purpose: Ovarian cancer is a leading cause of death among gynaecological malignancies. Transforming growth factor-beta 1 (TGF β1) and interleukin-10 (IL-10) are cytokines in the tumour microenvironment and may play critical roles in immune suppression. This study highlights these roles and immunosuppressive functions in epithelial ovarian cancer (EOC).
Methods: TGF-β1 and IL-10 expression was compared in malignant, benign, and borderline cancerous tissues and tumour-free tissue by immunohistochemistry. Relationships among the levels of these cytokines, correlation of expression level with EOC prognosis, and cytokine involvement in immunosuppression were investigated.
Results: Immunohistochemical analysis of TGF-β1 and IL-10 in epithelial cells showed the presence of epithelial, borderline, and benign ovarian tumour growth, and normal ovarian growth. TGF-β1 (P = 0.121), residual tumour after surgery (P = 0.231) and standard chemotherapy (P = 0.121) were prognostic factors for EOC. There were no significant differences in clinicopathologic factors between specimens expressing TGF-β1 at low and high levels, indicating that TGF-β1 is an independent factor in EOC diagnosis. Higher concentrations of TGF-β1 (1754.690 ± 3416.487 pg/ml) and IL 10 (2731.7101 ± 6.1613 pg/ml) were observed in A2780-conditioned than in control medium.
Conclusion: TGF-β1 and IL-10 play pivotal roles in EOC and can lead to immune evasion. Targeting these cytokines for tumour treatment, specifically at early stages, may prevent tumour progression.
Keywords: Epithelial ovarian cancer, TGF-β1, IL-10, histopathology
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.