Background
Ovarian cancer is usually diagnosed at an advanced stage due to its early asymptomatic course and late-stage non-specific symptoms. This highlights the importance of researching the molecular mechanisms involved in ovarian carcinogenesis as well as the discovery of novel prognostic markers that could help improve the survival outcome of patients. The aim of this study was to evaluate the expression of the steroid sulfatase (STS) in 154 samples of primary ovarian tumors. This protein is crucial in the intracellular conversion of sulfated steroid hormones to active steroid hormones. The presence of STS, 3β-HSD, and 17β-HSD1 result in the production of testosterone which act through the androgen receptor (AR) in the tumor cell. The presence of STS and AR in epithelial ovarian tumors and their association to the overall survival of patients was evaluated using Kaplan–Meier and Cox regression analyses.
Results
Immunoreactivity for STS was detected in 65% of the tumors and no association was observed with histological subtypes and clinical stages of the tumor. The STS expression in the tumors exhibiting immunoreactive AR resulted in a reduced survival (log-rank test, p = 0.032) and a risk factor in univariate and multivariate analysis, HR = 3.46, CI95% 1.00–11.92, p = 0.049 and HR = 5.92, CI95% 1.34–26.09, p = 0.019, respectively.
Conclusions
These findings suggest that the intracellular synthesis of testosterone acting through its receptor can promote tumor growth and progression. Moreover, the simultaneous expression of STS and AR constitutes an independent predictor of poor prognosis in epithelial ovarian tumors.
Multiple sclerosis (MS) is a chronic demyelinating and neurodegenerative disease that affects the central nervous system. MS is a heterogeneous disorder of multiple factors that are mainly associated with the immune system including the breakdown of the blood-brain and spinal cord barriers induced by T cells, B cells, antigen presenting cells, and immune components such as chemokines and pro-inflammatory cytokines. The incidence of MS has been increasing worldwide recently, and most therapies related to its treatment are associated with the development of several secondary effects, such as headaches, hepatotoxicity, leukopenia, and some types of cancer; therefore, the search for an effective treatment is ongoing. The use of animal models of MS continues to be an important option for extrapolating new treatments. Experimental autoimmune encephalomyelitis (EAE) replicates the several pathophysiological features of MS development and clinical signs, to obtain a potential treatment for MS in humans and improve the disease prognosis. Currently, the exploration of neuro-immune-endocrine interactions represents a highlight of interest in the treatment of immune disorders. The arginine vasopressin hormone (AVP) is involved in the increase in blood−brain barrier permeability, inducing the development and aggressiveness of the disease in the EAE model, whereas its deficiency improves the clinical signs of the disease. Therefore, this present review discussed on the use of conivaptan a blocker of AVP receptors type 1a and type 2 (V1a and V2 AVP) in the modulation of immune response without completely depleting its activity, minimizing the adverse effects associated with the conventional therapies becoming a potential therapeutic target in the treatment of patients with multiple sclerosis.
Epithelial ovarian cancer (EOC) is the most common and lethal of the ovarian neoplasms, frequently it is detected at advanced stages of the disease resulting in 60–70% of the cases in recurrence and less responsive to chemotherapy. Currently the role played by the neurohypophyseal hormone arginine vasopressin (AVP) and its receptors in the development of EOC is unknown. The purpose of this study was to evaluate the action of desmopressin (DDAVP), an AVP V2 receptor agonist on the cell proliferation and cell migration in cells from the OV‐90 cell line. Cell proliferation was evaluated with the proliferation marker Ki67, whereas the cells migration was evaluated by the wound assay. The AVP V1a and V2 receptors expression were assessed by immunofluorescence. Cell cultures were stimulated during 12, 24, 36 and 48 hours with DDAVP (500 to 1500 mM). In order to discard the cytotoxicity of DDAVP on the OV‐90 cell cultures in control and stimulated cultures the Cytotox 96 kit was used. The experiments were performed three times by duplicate. The results showed that the expression of AVP V1a and V2 receptors are present in both DDAVP stimulated and‐non stimulated cultures. On the other hand in comparison with the control cultures, doses of 1000mM of DDAVP significantly (p<0.05) inhibit both cell proliferation and cellular migration. Present results also suggests a possible inhibitory role of DDAVP on proliferation and cellular migration in the OV‐90 cell lines of epithelial ovarian cancer.
Support or Funding Information
Universidad Autónoma de Aguascalientes PIFF14‐1 and CONACYT 221262. México
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