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International Journal of Reproductive BioMedicine
Research and Clinical Center for Infertility, Shahid Sadoughi University of Medical Sciences of Yazd
ISSN: 1680-6433 EISSN: 1680-6433
Vol. 11, No. 11, 2013, pp. 919-924
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Bioline Code: rm13117
Full paper language: English
Document type: Research Article
Document available free of charge
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International Journal of Reproductive BioMedicine, Vol. 11, No. 11, 2013, pp. 919-924
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The expression of Toll-Like Receptors (TLRs) in testicular cancer: A case control study
Shapouri, Farnaz; Saeidi, Shaghayegh; Kakhki, Sara Ashrafi; Pouyan, Omid; Amirchaghmaghi, Elham & Aflatoonian, Reza
Abstract
Background: It has been suggested that malfunction of immune system may causes testicular cancer. Recently, our understanding of innate immune system has been expanded, by discovery of “Toll-Like Receptors” (TLRs). Some studies have shown that polymorphisms of TLR2 and 4 may affect on the risk of cancer. Also, the role of TLRs 3 and 9 have been shown in apoptosis and metastasis of cancer cells in animal models. Objective: Little information is available about the influence of innate immunity on testicular malignancy. Therefore, expression of TLRs 2, 3, 4 and 9 as main components of innate immunity has been investigated in this study. Materials and Methods: In this case control study, TLRs gene expression was examined by RT-PCR in normal testis and testicular cancer tissues. Real time quantitative PCR (Q-PCR) analysis was used to compare the relative expression of TLRs between the samples. Results: mRNAs of TLR 2, 3, 4 and 9 were expressed in all normal and cancer samples. Q-PCR reveals that cancer samples had stronger expression of these genes compared with normal ones. Conclusion: It seems that the different TLRs expression in testicular cancer cells may contribute to extensive signaling pathways involved in carcinogenesis.
Keywords
Toll- like Receptors (TLRs); Testicular Cancer; Innate Immunity; NF-kappa B
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© Iranian Journal of Reproductive Medicine Alternative site location: http://www.ijrm.ir
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