Loss of EMP1 promotes the metastasis of human bladder cancer cells by promoting migration and conferring resistance to ferroptosis through activation of PPAR gamma signaling.

Metastasis, in which cancer cells detach from the original site and colonise other organs, is the primary cause of death induced by bladder cancer (BCa). Epithelial Membrane Protein 1 (EMP1) is dysregulated in many human cancers, and its clinical significance and biological function in diseases, including BCa, are largely unclear. Here, we demonstrated that EMP1 was downregulated in BCa cells.

RAC3 Inhibition Induces Autophagy to Impair Metastasis in Bladder Cancer Cells the PI3K/AKT/mTOR Pathway.

Background: Bladder cancer (BCa) is one of the most frequent malignant tumors globally, with a significant morbidity and mortality rate. Gene expression dysregulation has been proven to play a critical role in tumorigenesis. Ras-related C3 botulinum toxin substrate3 (RAC3), which is overexpressed in several malignancies and promotes tumor progression, has been identified as an oncogene.

Attenuated expression of SNF5 facilitates progression of bladder cancer via STAT3 activation.

Background: SWI/SNF, a well-known ATP-dependent chromatin-remodeling complex, plays an essential role in several biological processes. SNF5, the core subunit of the SWI/SNF remodeling complex, inactivated in 95% of malignant rhabdoid tumors (MRT), highlighting its significance in tumorigenesis. However, the role of SNF5 in bladder cancer (BC) remains unknown.

Prostatic fluid exosome-mediated microRNA-155 promotes the pathogenesis of type IIIA chronic prostatitis.

Background: The latest research has shown that exosomes play an important role in cell-to-cell communication and are closely related to the occurrence of many chronic inflammatory diseases. However, no studies have clarified whether exosomes are involved in the pathogenesis of aseptic inflammation, type IIIA chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS-A). This study aimed to explore the relationship between prostatic fluid exosomes and CP/CPPS-A and reveal new pathogenesis.

Association Between the Incidence of Pancreatic Fistula After Pancreaticoduodenectomy and the Degree of Pancreatic Fibrosis.

Objective: The objective of this study is to investigate the association between the incidence of pancreatic fistula after pancreaticoduodenectomy (PD) and the degree of pancreatic fibrosis.

Method: Between January 2013 and December 2016, the analysis of the clinical data of 529 cases of pancreaticoduodenectomy patients of our hospital was performed in a retrospective fashion. The univariate analysis and multivariate analysis were done using the Pearson chi-squared test and binary logistic regression analysis model; correlations were analyzed by Spearman rank correlation analysis.

4,4'-Diisothiocyanostilbene-2,2'-disulfonic Acid (DIDS) Ameliorates Ischemia-Hypoxia-Induced White Matter Damage in Neonatal Rats through Inhibition of the Voltage-Gated Chloride Channel ClC-2.

Chronic cerebral hypoperfusion is believed to cause white matter lesions (WMLs), leading to cognitive impairment. Previous studies have shown that inflammation and apoptosis of oligodendrocytes (OLs) are involved in the pathogenesis of WMLs, but effective treatments have not been studied. In this study, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), a chloride (Cl-) channel blocker, was injected into chronic cerebral ischemia-hypoxia rat models at different time points.

Vinyl chloride monomer (VCM) induces high occurrence of neural tube defects in embryonic mouse brain during neurulation.

The aim of this study was to explore the direct embryonic teratogenicity of vinyl chloride monomer (VCM), especially the toxic effects on the early development of the nervous system and its underlying mechanisms. Pregnant mice at embryonic day 6.5 (E6.