Prostate cancer (PC), which has high morbidity and mortality among elderly men, is becoming the most common malignancy in men. The progression of PC is associated with several aspects including apoptosis, proliferation and metastasis. C-Jun N-terminal kinase (JNK) is a member of mitogen-activated protein kinases (MAPKs), which play vital roles in regulating diverse cell processes. JNK has been shown to activate multiple substrates to modulate apoptosis, proliferation, tumorigenesis and inflammation in response to various stimuli including cytokines, pathogens, growth factors, oxidative stress, ultraviolet radiation, toxins and drugs. In addition, emerging evidence has indicated the significant roles of androgen receptor in prostate cancer development. In this review, we will summarize our current knowledge on the roles of JNK in the apoptosis, proliferation, migration and DNA repair as well as dissect the relationships between JNK and androgen receptor in prostate cancer. Chemotherapeutic drugs targeting JNK will also be discussed, possibly providing an overview on the development of therapeutic strategies.

Metastatic castration-resistant prostate cancer (mCRPC) is one of the main contributors to the death of prostate cancer patients. To date, the detailed molecular mechanisms underlying mCRPC are unclear. Given the crucial role of epithelial–mesenchymal transition (EMT) in cancer metastasis, we aimed to analyse the expression and function of Transforming growth factor-beta (TGF-β) signal-associated protein named Sox5 in mCRPC. The protein expression levels were analysed by western blot, immunohistochemistry and immunofluorescence. Luciferase reporter assays and chromatin immunoprecipitation were employed to validate the target of Sox5. The effect of Smad3/Sox5/Twist1 on PCa progression was investigated in vitro and in vivo. Here, we found that TGF-β-induced EMT was accompanied by increased Sox5 expression. Interestingly, knockdown of Sox5 expression attenuated EMT induced by TGF-β signalling. Furthermore, we demonstrated that Smad3 could bind to the promoter of Sox5 and regulate its expression. Mechanistically, Sox5 could bind to Twist1 promoter and active Twist1, which initiated EMT. Importantly, knockdown of Sox5 in prostate cancer cells resulted in less of the mesenchymal phenotype and cell migration ability. Furthermore, targeting Sox5 could inhibit prostate cancer progression in a xenograft mouse model. In clinic, patients with high Sox5 expression were more likely to suffer from metastases, and high Sox5 expression also has a lower progression-free survival and cancer specific-survival in clinic database. Therefore, we propose a new mechanism in which Smad3/Sox5/Twist1 promotes EMT and contributes to PCa progression.

Objective: To compare the prognosis of papillary and clear cell renal cell carcinoma (RCC) in order to determine the optimal follow-up and therapy for patients with RCC. Methods: A systematic search of Web of Science, EMBASE, Cochrane Library, and PubMed databases was conducted for articles published through July 30, 2018, reporting on a comparison of the prognosis of papillary RCC and clear cell RCC using the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. Results: Of 1896 studies, 11 were considered for the evidence synthesis. A total of 35,832 patients were included. Of these patients, 6907 patients were diagnosed with papillary renal cell carcinoma, and 28,925 patients were diagnosed with clear cell renal cell carcinoma. The prognosis of papillary RCC was better than that of clear cell RCC (hazard ratio (HR) = 0.50; 95% confidence interval (CI) 0.45 to 0.56; P < .001; I ² = 91.9%). A subgroup analysis indicated that papillary RCC was associated with better outcomes (HR = 0.76, 95% CI 0.50–1.16), and a trend toward a higher risk of mortality was observed in patients with metastatic RCC presenting with papillary histology, but the difference was not statistically significant (HR = 1.12, 95% CI 0.71–1.76, P = .085). Pooled data suggested a lack of a significant difference between papillary RCC (p-RCC) type 1 and clear cell RCC (cc-RCC) (HR = 0.30, 95% CI 0.12–0.73, P = .085). The pooled HR for the prognosis of p-RCC type 2 compared to cc-RCC was 1.69 (95% CI 0.93–3.08; P = .032). Conclusion: Papillary RCC is associated with better outcomes than clear cell RCC in patients without metastases, but not in patients with metastases. Optimal follow-up or therapy for patients with RCC should be assigned according to the tumor stage and subtype.

To compare the standard percutaneous nephrolithotomy and mini-percutaneous nephrolithotomy in order to determine the optimal tract size for patients with renal stones. A systematic search of Web of Science, EMBASE, Cochrane Library, and PubMed databases was conducted for articles published through 20 August 2019, reporting on a comparison of the standard percutaneous nephrolithotomy and mini-percutaneous nephrolithotomy using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Of 763 studies, 14 were considered for the evidence synthesis. A total of 1980 cases were included. Of these patients, 897 cases underwent standard percutaneous nephrolithotomy, and 1083 cases underwent mini-percutaneous nephrolithotomy. Stone-free rates were 87.6% (786 of 897 patients) for standard percutaneous nephrolithotomy and 87.8% (951 of 1083 patients) for mini-percutaneous nephrolithotomy (p = 0.57). Tract sizes of 30F and 22–26F in standard percutaneous nephrolithotomy group shorten operation time compared with mini-percutaneous nephrolithotomy (p = 0.02; p = 0.004; respectively). Leakage (p = 0.04), bleeding (p = 0.01), blood transfusion (p < 0.00001), and renal pelvis perforation (p = 0.02) were more common in standard percutaneous nephrolithotomy group than in mini-percutaneous nephrolithotomy group. Subgroup analysis showed only blood transfusion for 30F and 22–26F standard percutaneous nephrolithotomy group was more common than mini-percutaneous nephrolithotomy (p < 0.0001, p = 0.005, respectively). Standard percutaneous nephrolithotomy was associated with higher leakage, bleeding, blood transfusion, and renal pelvis perforation, but had a shorter operation time. Tract size of 30F improved the stone-free rate compared with mini-percutaneous nephrolithotomy, but led to more complications. Tract size of 22–26F was no better than 30F or mini-percutaneous nephrolithotomy.

Ongoing efforts are focused on shortening ischemia intervals as much as possible during partial nephrectomy to preserve renal function. Off-clamp partial nephrectomy (off-PN) has been a common strategy for to avoid ischemia in small renal tumors. Although studies comparing the advantages between off-PN with conventional on-clamp partial nephrectomy (on-PN) have been reported, the impact on short- and especially long-term renal function of the two surgical methods has not been discussed seriously and remained unclear. Our purpose is to evaluate the impact on short- (within postoperative 3 months) and long-term (postoperative 6 months or longer) renal function of off-PN compared with that of on-PN. We comprehensively searched databases, including PubMed, EMBASE, and the Cochrane Library, without restrictions on language or region. A systematic review and cumulative meta-analysis of the included studies were performed to assess the impact of the two techniques on short- and long-term renal function. A total of 23 retrospective studies and 2 prospective cohort studies were included. The pooled postoperative short-term decrease of estimated glomerular filtration rate (eGFR) was significantly less in the off-PN group (weighted mean difference [WMD]: 4.81 ml/min/1.73 m2; 95% confidence interval [CI]: 3.53 to 6.08; p < 0.00001). The short-term increase in creatinine (Cr) level in the on-PN group was also significant (WMD: − 0.05 mg/dl; 95%CI: − 0.09 to − 0.00; p = 0.04). Significant differences between groups was observed for the long-term change and percent (%) change of eGFR (p = 0.04 and p < 0.00001, respectively) but not for long-term Cr change (p = 0.40). The postoperative short-term eGFR and Cr levels, but not the postoperative long-term eGFR, differed significantly between the two groups. The pooled odds ratios for acute renal failure and postoperative progress to chronic kidney disease (stage≥3) in the off-PN group were found to be 0.25 (p = 0.003) and 0.73 (p = 0.34), respectively, compared with the on-PN group. Off-PN exerts a positive impact on the short- and long-term renal function compared with conventional on-PN. Given the inherent limitations of our included studies, large-volume and well-designed RCTS with extensive follow up are needed to confirm and update the conclusion of this analysis.

Androgen receptor plays a pivotal role in prostate cancer progression, and androgen deprivation therapy to intercept androgen receptor signal pathway is an indispensable treatment for most advanced prostate cancer patients to delay cancer progression. However, the emerging of castration-resistant prostate cancer reminds us the alteration of androgen receptor, which includes androgen receptor mutation, the formation of androgen receptor variants, and androgen receptor distribution in cancer cells. In this review, we introduce the process of androgen receptor and also its variants’ formation, translocation, and function alteration by protein modification or interaction with other pathways. We dissect the roles of androgen receptor in prostate cancer from molecular perspective to provide clues for battling prostate cancer, especially castration-resistant prostate cancer.