TRIM/RBCC are a large family of proteins that include more than 80 proteins, most of which act as E3 ligases and catalyze the direct transfer of Ubiquitin, SUMO and ISG15 on specific protein substrates. They are involved in oncogenesis processes and in cellular immunity. On this topic, we focus on TRIM8 and its multiple roles in tumor pathologies. TRIM8 inhibits breast cancer proliferation through the regulation of estrogen signaling. TRIM8 downregulation in glioma is involved in cell proliferation, and it is related to patients’ survival. Several studies suggested that TRIM8 regulates the p53 suppressor signaling pathway: it is involved in the NF-kB pathway (Nuclear Factor kappa light- chain-enhancer of activated B cells) and in STAT3 (Signal Transducer and Activator of Transcription 3) of the JAK-STAT pathway. In this review, we summarize how the association between these different pathways reflects a dual role of TRIM8 in cancer as an oncogene or a tumor suppressor gene.

Background: The impact of metabolic syndrome on female sexual dysfunction received modest consideration in clinical practice. The aim of the research was to analyze the international literature to determine the relationship between the metabolic syndrome, its components and female sexual disorders. Methods: We identified relevant full-length papers by electronic databases as Index Medicus/Medline, Scopus, Life Science Journals, from 2005 to the present. Studies were searched using the following as search query: metabolic syndrome, female sexual dysfunction, obesity, systemic arterial hypertension, diabetes mellitus, dyslipidemia. Results: Women with metabolic syndrome showed higher prevalence of sexual inactivity and low sexual desire, orgasm and satisfaction respect to women without metabolic syndrome. Particularly metabolic components as diabetes mellitus, dy-slipidemia, systemic arterial hypertension were strongly associated with lower sexual desire, activity and Female Sexual Function Index total score. In contrast, other studies showed no relationship. Conclusion: Our study showed that in the clinical evaluation of women with metabolic syndrome routine inquiring about female sexual dysfunction should be recommended to ameliorate sexual function and quality of life. However more prospective and longitudinal studies on the sexual effects of metabolic syndrome should also be suggested to know the factors related to women's sexuality better.

Background: Epidemiological studies suggest a possible relationship between metabolic alterations, cardiovascular disease and aggressive prostate cancer, however, no clear consensus has been reached. Objective: The aim of the study was to analyze the recent literature and summarize our experience on the association between metabolic disorders, aggressive hormone-naïve prostate cancer and cardiovascular disease. Method: We identified relevant papers by searching in electronic databases such as Scopus, Life Science Journals, and Index Medicus/Medline. Moreover, we showed our experience on the reciprocal relationship between metabolic alterations and aggressive prostate cancer, without the influence of hormone therapy, as well the role of coronary and carotid vasculopathy in advanced prostate carcinoma. Results: Prostate cancer cells have an altered metabolic homeostatic control linked to an increased aggressivity and cancer mortality. The absence of discrimination of risk factors as obesity, systemic arterial hypertension, diabetes mellitus, dyslipidemia and inaccurate selection of vascular diseases as coronary and carotid damage at initial diagnosis of prostate cancer could explain the opposite results in the literature. Systemic inflammation and oxidative stress associated with metabolic alterations and cardiovascular disease can also contribute to prostate cancer progression and increased tumor aggressivity. Conclusions: Metabolic alterations and cardiovascular disease influence aggressive and metastatic prostate cancer. Therefore, a careful evaluation of obesity, diabetes mellitus, dyslipidemia, systemic arterial hypertension, together with a careful evaluation of cardiovascular status, in particular coronary and carotid vascular disease, should be carried out after an initial diagnosis of prostatic carcinoma.

In this review we analyzed the role of PGE2 as a possible regulator of bone metabolism and bone metastases in prostate cancer. Published studies were identified by searching computerized bibliographic systems from January 1(st), 2000 to July 1(st), 2011. PGE2 represents a key factor in the modulation of bone metabolism and bone metastatic disease in prostate cancer interacting with bone regulatory signals including the RANK/RANKL/OPG system and Wnt pathways. A high concentration of PGE2 exerts a prevalent stimulatory effect on osteoclastogenesis via OPG/RANK/RANKL axis activation and a inhibitory effect on osteoblastogenesis trough inhibition of Wnt pathway. An inversely low level of PGE2 exerts a stimulatory effect on osteoblastogenesis via activation of the Wnt pathway. Our finding suggests that PGE2 acts as a regulator in maintaining normal bone mass and indicate a mechanism whereby chemical manipulation of PGE2 levels or signaling may be therapeutically beneficial for prostate cancer treatment.

Epidemiologic studies have implicated obesity in prostate cancer (PCa) development and aggressiveness; nevertheless, no clear consensus has been reached. The aim of the research was to investigate the association of obesity with PCa, hormone-naïve at initial diagnosis. A retrospective analysis of 266 patients undergoing prostate biopsy at our institution, between 2006 and 2009, was conducted. We examined obesity and PCa association in 133 patients with PCa, hormone-naïve at initial diagnosis, versus 133 age-matched controls. Men with incomplete data available, a history of hormone therapy or chemotherapy, prostate or bladder surgery were excluded. Obesity was significantly associated (OR 2.25) with aggressive PCa (Gleason score ≥7) and inversely related (OR 0.35) to non-aggressive PCa (Gleason score ≤6). Particularly, obesity in diabetic patients was significantly linked with aggressive PCa (OR 4.17). No association was noted between obesity and PCa development. In our study, obese patients, particularly in combination with diabetes mellitus (DM), were more likely to present with more aggressive PCa. Further research with larger samples should be done to confirm these associations and to stabilize future prevention strategies.

The Central European Journal of Urology is an open access quarterly-issued journal, which provides a forum for the presentation of original clinical, experimental and other research studies...