Apoptosis induction in Jurkat cells and sCD95 levels in women's sera are related with the risk of developing cervical cancer

Jurkat cells were exposed to serum from 63 women (20 healthy volunteers, 21 with cervical intraepithelial neoplasia grade I [CIN 1] and 22 with cervical-uterine carcinoma). The apoptotic rate was measured by flow cytometry using Annexin-V-Fluos and Propidium Iodide as markers. Serum levels of sCD95 and soluble CD95 ligand (sCD95L) were measured by ELISA kits.We found that serum from almost all healthy women induced apoptosis in Jurkat cells, while only fifty percent of the sera from women with CIN 1 induced cell death in Jurkat cells. Interestingly, only one serum sample from a patient with cervical-uterine cancer was able to induce apoptosis, the rest of the sera protected Jurkat cells from this killing. We were able to demonstrate that elimination of Jurkat cells was mediated by the CD95/Fas/Apo-1 apoptotic pathway. Furthermore, the serum levels of sCD95 measured by ELISA were significantly higher in women with cervical cancer.Our results demonstrate that there is a strong correlation between low levels of sCD95 in serum of normal women and higher apoptosis induction in Jurkat cells. We suggest that an analysis of the apoptotic rate induced by serum in Jurkat cells and the levels of sCD95 in serum could be helpful during the prognosis and treatment of women detected with precancerous lesions or cervical cancer.A balance between apoptosis and cell proliferation are crucial features for the maintenance of homeostasis in multicellular organisms [1]. In malignant cells, apoptotic pathways are often disturbed, leading to uncontrollable growth and to resistance to anti-tumor treatment [2,3]. It is now well established that apoptosis plays an important role in the regulation of tumor progression [4,5]. Diverse molecular mechanisms, such as overexpression of anti-apoptotic proteins, inactivation of death receptors and mutations or epigenetic regulation of tumor suppressor genes, have been implicated in the failure of apoptosis in tumor cells [6-8].Anti-apoptotic factors a