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Circular RNA DDX17 (circDDX17) has been demonstrated as a tumor suppressor in colorectal cancer. However, mechanisms underlying circDDX17 effects in cases of prostate cancer (PCa) are not well understood. Thus, herein, we determined measures of circDDX17 expression by use of the TCGA database. Expression of circDDX17 in prostate cancer-afflicted tissue samples was determined by qRT-PCR. Functionally, circDDX17 induced remarkable inhibition of cell colonizing ability, invasion, and epithelial-mesenchymal transition (EMT) progression in vitro. Mechanistically, dual-luciferase reporter assays, RNA immunoprecipitation, and RNA pull-down experiments helped verify interactions between circDDX17 and miR-346. Low expression of circDDX17 occurred in TCGA PCa samples. Furthermore, circDDX17 expression was downregulated significantly in PCa. These results suggested that circDDX17 suppressed PC cell mobility, proliferation, and invasion. Mechanistic experiments indicated that circDDX17 might serve as a ceRNA of miR-346 to relieve repressive effects of miR-346 upon phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP). LHPP expression itself was downregulated in TCGA PCa samples. Overall, our findings indicated that the circDDX17/miR-346/LHPP pathway inhibited the progression of prostate cancer and that circDDX17 may be a new potential therapeutic or diagnostic target for treating and diagnosing prostate cancer. As our study also demonstrated for the first time that LHPP might act as an anticancer gene in prostate cancer, the findings could have wide-ranging implications for the treatment of this affliction.

Purpose: The prognostic value of obesity in patients with renal cell carcinoma (RCC) remains controversial. This study aimed to assess the sex-dependent prognostic role of body mass index (BMI) in patients with nonmetastatic RCC who underwent radical or partial nephrectomy. Patients and methods: We retrospectively analyzed 643 consecutive patients with nonmetastatic RCC who underwent curative nephrectomy in our center between 2004 and 2014. Associations among BMI, sex, overall survival (OS), cancer-specific survival (CSS), and metastasis-free survival (MFS) were analyzed. Results: Males were more likely to have a higher BMI than females (BMI as a categorical variable: P <0.001; BMI as a continuous variable: P =0.002). In men, a high BMI was significantly correlated with better 5-year OS, CSS, and MFS rates ( P =0.001, 0.014, and 0.001, respectively), and multivariate analysis identified that a high BMI was independently associated with greater OS, CSS, and MFS (OS: hazard ratio [HR]=0.207, P =0.011; CSS: HR=0.225, P =0.005; MFS: HR=0.243, P =0.004). However, in women, there was no significant difference in 5-year OS, CSS, and MFS rates according to BMI ( P =0.781, 0.812, and 0.538, respectively). Moreover, a high BMI was no longer independently associated with OS, CSS, or MFS ( P =0.821, 0.832, and 0.801, respectively). Among patients with clear cell RCC, BMI was significantly associated with OS, CSS, and MFS only among men (all P <0.05) and not among women (all P >0.05). Conclusion: Among patients with nonmetastatic RCC, a high BMI was a favorable prognostic factor in males rather than females. Therefore, sex might influence the correlation between obesity and urological outcomes in nonmetastatic RCC.

Background To develop a nomogram to predict cancer-specific survival (CSS) in patients with metastatic testicular germ cell tumors (mTGCTs). Methods Data were obtained from the Surveillance, Epidemiology, and End Results database. Univariate and multivariate Cox regression models were used to identify factors associated with CSS. Survival times between different groups were compared using Kaplan-Meier survival curves and the log-rank test. A nomogram visualization model was established using the R language to predict survival rates. Harrell’s concordance index (C-index), the area under the receiver operating characteristic curve (AUC) and calibration plots were used to assess the performance of the model. Results We analyzed the data of 949 patients. The median follow-up time was 32 months (range 0 to 83 months), and 224 (23.60%) patients died before the last follow-up, of whom 193 (20.33%) died of mTGCTs. The site of distant metastases was an independent prognostic factor for CSS. Compared to patients without involvement of the corresponding organ, patients with bone, brain, liver, and lung involvement had worse CSS. We also found that age, histological type, surgery, radiation therapy, chemotherapy, metastatic site and insurance status affected the CSS of patients with mTGCTs. We used these prognostic factors to construct our nomogram. Harrell’s C-index for CSS was 0.739. The AUC and calibration plots indicated good performance of the nomogram. Conclusions A nomogram for predicting CSS in patients with mTGCTs has been developed, which can help patients and clinicians accurately predict mortality risk and recommend personalized treatment modalities.

Background: To examine the association between age at diagnosis and cancer-specific mortality (CSM) in primary urachal adenocarcinoma. Methods:The data was obtained from the National Cancer Institute's Surveillance, Epidemiology, and End Results program (SEER). A total of 393 patients were included in the study. Smooth curve fitting and two-piecewise Cox proportional hazards models were used to identify the nonlinearity between the age at initial diagnosis and cancer-specific survival rate. Survival time between different groups was compared using Kaplan-Meier survival curves and the log-rank test.Results: Using smooth curve fitting we found that the relationship between age at diagnosis and cancerspecific survival takes on a U-shaped curve. The inflection point that we identified for the age at initial diagnosis was 60 years. The log-likelihood ratio test (P<0.05) indicated that the two-piecewise Cox regression model was more appropriate for fitting the correlation of age at diagnosis and CSM. The two-piecewise Cox regression model showed that when the age was <60 years, reduced risk of CSM was significantly associated with increased age (HR: 0.95, P=0.0002). Conversely, when age was >60 years, increased risk of CSM was significantly associated with increased age (HR: 1.05, P=0.0499).Conclusions: In summary, our study suggested that the relationship between age at diagnosis and cancerspecific survival is nonlinear, and takes on a U-shaped curve. Both younger and older age at initial diagnosis age were associated with increased CSM.