Previous studies have demonstrated that the expression of CARD10 is closely associated with the occurrence of tumors, and its role is mainly to promote tumor progression by activating the transcription factor NF-κB. However, the signaling pathway in renal cancer remains unclear. The objective of the present study was to investigate the ability of caspase recruitment domain 10 (CARD10) to regulate the NF-κB signaling pathway and promote the progression of renal cell carcinoma (RCC). Expression of CARD10 in ACHN, 786-O and HK-2 cells was evaluated via western blot analysis, as was the epidermal growth factor (EGF)-induced activation of NF-κB signaling pathway-related proteins in cells. The expression of CARD10 was inhibited by CARD10 short hairpin RNA transfection. Cell cycle analysis and MTT assays were used to evaluate cell proliferation. Cell apoptosis was analyzed via flow cytometry. The invasion of renal cell lines was detected via Transwell cell migration and invasion assays in vitro. The results showed that CARD10 expression was significantly higher in RCC cells than in normal renal tubular epithelial cells. CARD10 silencing inhibited the proliferation, invasion and migration of RCC cells. EGF stimulation upregulated the activation of the NF-κB pathway in RCC cells. Inhibition of CARD10 expression inhibited NF-κB activation in RCC cells. Taken together, these data suggested that CARD10 promotes the progression of renal cell carcinoma by regulating the NF-κB signaling pathway. Thus, this indicated that CARD10 may be a novel therapeutic target in RCC.

No abstract

Renal cell carcinoma (RCC) is a lethal urologic tumor commonly seen in men that best responds to partial nephrectomy. An enhanced understanding of the molecular pathogenesis of RCC can broaden treatment options and tumor prevention strategies. Sirtuin 1 (SIRT1) is a NAD+-dependent deacetylase that regulates several bioactive substances, and the present study aimed to identify the role of SIRT1/AMP-activated protein kinase (AMPK) signaling in RCC progression. SIRT1 expression was detected in 100 patients with RCC using tissue microarray immunohistochemistry. SIRT1-knockdown and overexpression were performed via RNA interference and plasmid transfection. Inhibition of AMPK was used for the phenotypic rescue assays to verify whether AMPK was a downstream target of SIRT1. Reverse transcription-quantitative PCR was performed to verify transfection efficiency. Transwell, MTT and flow cytometry apoptosis assays were performed to evaluate the migration, invasion, proliferation and early apoptosis level of RCC cells. SIRT1 and AMPK protein expression in human RCC tissues and cell lines (786-O and ACHN) was detected using western blotting and immunofluorescence staining. The current results, combined with data from The Cancer Genome Atlas database, revealed that SIRT1 expression in RCC tissues was downregulated compared with in adjacent normal tissues. Additionally, high SIRT1 expression was associated with an improved prognosis in patients with RCC. Overexpression of SIRT1 inhibited the proliferation, migration and invasion of RCC cell lines and induced apoptosis, while inhibition of SIRT1 expression had the opposite effects. Further experiments indicated that SIRT1 may serve an anticancer role by upregulating the expression levels of downstream AMPK, thus revealing a potential therapeutic target for RCC.

There have been some conflicting claims whether larger prostate weight (PW) reduces the risk of positive surgical margins (PSMs). This study aims to examine the associations between PW and PSMs. PubMed, Web of Science and Cochrane library were systematically retrieved. Relative risks (RRs) and the corresponding 95% confidence intervals (CIs) were synthesised utilising random‐effect models. Ultimately, 22 cohort studies met criteria were enrolled in this meta‐analysis, of which 18 studies reporting the RR of the highest VS lowest category of PW yielded the combined RR of PSMs of 0.61 (95% CI 0.50–0.74). Subgroup analysis showed that geographic region and surgical modalities were considered as potential confounders of influence of PW on PSMs. The nonlinear dose–response relationship demonstrated that PSM risk decreased by 1% (RR = 0.99, 95% CI, 0.98–0.99) for every one gram increment in PW. This study suggests PW has a negative association with risk of PSMs, and having a appropriate PW is very important.

Background: To explore the risk factors that lead to the formation of bladder calculus in patients with benign prostatic hyperplasia (BPH). Methods: Retrospective study was performed between June 2017 and October 2019, 103 patients with BPH who underwent transurethral resection of the prostate (TURP) were included. Patients with BPH were divided into two groups: 32 patients with bladder calculus in group1 and 71 patients without bladder calculus in group2. Characteristics of both groups were compared and univariate and multivariate analyses were performed to investigate the association between BPH with or without bladder calculus. Results: There was no significant difference between the two groups regarding age, duration of BPH, body mass index (BMI), total prostate volume (TPV), total prostate-specific antigen (TPSA), International prostate symptom score (IPSS), serum albumin, hemoglobin, uric acid, urinary tract infection, diabetes, and hypertension. The patients' serum creatinine and acute urinary retention (AUR) were significantly lower, while intravesical prostatic protrusion (IPP) was significantly higher in group 1 than group 2. Multivariate analyses revealed that IPP and AUR were significant risk factors for the formation of bladder calculus in patients with BPH. For IPP, the receiver operating characteristic (ROC) curve showed that the cut-off value of the highest risk of the formation of bladder calculus was 11.5 mm. Conclusions: Our study indicated that IPP and AUR were independent risk factors that were closely linked with the incidence of bladder calculus in BPH patients.