A genetic study to identify pathogenic mechanisms and drug targets for benign prostatic hyperplasia: a multi-omics Mendelian randomization study.

Benign prostatic hyperplasia (BPH) as a common geriatric disease in urology, the incidence and prevalence are rapidly increasing with the aging society, prompting an urgent need for effective prevention and treatment of BPH. However, limited therapeutic efficacy and higher risk of complications result in the treatment of BPH remaining challenging. The unclear pathogenic mechanism also hampers further exploration of therapeutic approaches for BPH.

A Large Genetic Causal Analysis of the Gut Microbiota and Urological Cancers: A Bidirectional Mendelian Randomization Study.

Background: Several observational studies and clinical trials have shown that the gut microbiota is associated with urological cancers. However, the causal relationship between gut microbiota and urological cancers remains to be elucidated due to many confounding factors.

Methods: In this study, we used two thresholds to identify gut microbiota GWAS from the MiBioGen consortium and obtained data for five urological cancers from the UK biobank and Finngen consortium, respectively.

Assessment of an exhaled breath test using ultraviolet photoionization time-of-flight mass spectrometry for the monitoring of kidney transplant recipients.

Continuous monitoring for immunosuppressive status, infection and complications are a must for kidney transplantation (KTx) recipients. Traditional monitoring including blood sampling and kidney biopsy, which caused tremendous medical cost and trauma. Therefore, a cheaper and less invasive approach was urgently needed.

Circ_0057558 accelerates the development of prostate cancer through miR-1238-3p/SEPT2 axis.

Background: Prostate cancer (PCa) is one of the most common malignant tumors in males with high morbidity and mortality. Existing studies have demonstrated that circ_0057558 may be a molecular marker affecting PCa. However, its detailed roles in PCa remain unclear.

A Ferroptosis-Related Gene Signature for Predicting Survival and Immunotherapy Effect in Renal Cancer.

Background: Most recently, no efficient prognostic indictor is present for kidney cancer. Thus, we aimed to build and validate a new prognostic gene signature for renal cancer patients using the Cancer Genomic Atlas (TCGA).

Methods: A "time-dependent receiver operating characteristic (tROC)" curve was generated, and a log-rank test was performed to assess the performance of the biomarker in training and validation.

Epigallocatechin-3-gallate induces autophagy-related apoptosis associated with LC3B II and Beclin expression of bladder cancer cells.

The incidence of bladder cancer in traditional green tea-consuming countries was dramatically lower than low green tea-consuming countries. Epigallocatechin-3-gallate (EGCG), an active ingredient extracted from green tea, showed effective inhibition of formation and progression of many tumors. However, whether autophagy involved in this tumor-suppression mechanism of EGCG on bladder cancer was still unclear.

Suppression of Cellular Proliferation and Invasion by HMGB1 Knockdown in Bladder Urothelial Carcinoma Cells.

HMGB1, which acts as a DNA chaperone to help maintain nuclear homeostasis, was reported to play a prominent role in cancer progression, angiogenesis, invasion, and metastasis development. Increased expression of HMGB1 has been observed in several tumor entities. However, the molecular mechanisms of HMGB1 in tumorigenesis of bladder cancer have rarely been reported.

microRNA-32 induces radioresistance by targeting DAB2IP and regulating autophagy in prostate cancer cells.

The aberrant expression of microRNAs (miRNAs/miRs) has been found in numerous cancer types. miR-32 is an oncomiR in prostate cancer (PCa), however, the mechanisms by which miR-32 functions as a regulator of radiotherapy response and resistance in PCa are largely unknown. In the present study, it was found that DAB2 interacting protein (DAB2IP), the miR-32-dependent tumor-suppressor gene, was downregulated and induced autophagy and inhibited radiotherapy-induced apoptosis in PCa cells.

Methylation-induced silencing of miR-34a enhances chemoresistance by directly upregulating ATG4B-induced autophagy through AMPK/mTOR pathway in prostate cancer.

miR-34a is downregulated and a regulator of drug resistance in prostate cancer (PCa). However, the mechanism of miR-34a in chemoresistance of PCa remains largely unknown. In the present study, we first confirmed the hypermethylation‑induced downregulation of miR-34a in PCa tissues and cell lines, PC-3 and DU145.