Anoikis-related genes signature development for clear cell renal cell carcinoma prognosis and tumor microenvironment.

Clear cell renal cell carcinoma (ccRCC) is one of the most common primary malignancies of the urinary tract, highly heterogeneous, and increasing in incidence worldwide. Anoikis is a specific type of programmed cell death in which solid tumor cells or normal epithelial cells that do not have metastatic properties lose adhesion to the extracellular matrix or undergo inappropriate cell adhesion-induced apoptosis. Anoikis is thought to play a critical role in tumorigenesis, maintenance, and treatment, according to an increasing amount of research. However, there is still some uncertainty regarding the general impact of anoikis-related genes (ARGs) on the prognostic importance, tumor microenvironment characteristics, and treatment reaction of ccRCC patients. For this study, we used The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus datasets to access the RNA sequencing results and clinical information from ccRCC patients. 29 ARGs related to survival were found using differential analysis and univariate Cox regression analysis. The samples were then divided into two clusters that had different immune traits via unsupervised cluster analysis using 29 prognosis-associated differently expressed ARGs. Then, to build an ARGs signature, 7 genes (PLAU, EDA2R, AFP, PLG, TUBB3, APOBEC3G, and MALAT1) were found using Least Absolute Shrinkage and Selection Operator regression analysis. The new ARGs signature demonstrated outstanding prognostic capability for ccRCC patients' overall survival. In conclusion, for ccRCC patients, we created an ARGs signature that strongly connects to immunological traits and therapy response. Clinicians may find this ARGs signature helpful in developing more individualized and detailed treatment strategies for ccRCC patients.

Antioxidant protein peroxiredoxin 6 suppresses the vascular inflammation, oxidative stress and endothelial dysfunction in angiotensin II-induced endotheliocyte.

Cardiovascular disease (CVD) states are associated with endothelial dysfunction (ED) and increased production of ROS in endothelial cells. The present study aimed to explore the protective effects of antioxidant protein peroxiredoxin 6 (PRDX6) on angiotensin II (AngII)­induced human umbilical vein endothelial cell (HUVEC) dysfunction. To investigate cell viability, levels of inflammatory molecules and proteins were assayed using the CCK-8 assay and evaluated by ELISA and Western blot. NO and ROS levels were determined by Griess assay and the fluorescent probe DCFH-DA. Cell migration capacity was assessed by Transwell assay. AngII decreased cell viability and PRDX6, upregulated the expression levels of TNF-α, IL-6, IL-1ß, LDH and MDA, stimulated ROS production, and reduced NO synthase, the expressions of eNOS, MnSOD, ICAM-1, VCAM-1, and activated the MAPK family of signaling proteins. However, the stimulatory effects of AngII on HUVECs were remarkably suppressed by PRDX6. Furthermore, mercaptosuccinate (MS; PRDX6 inhibitor) had similar effects as AngII in aggravating HUVECs damage. Conversely, these adverse events caused by AngII and MS were obviously reversed by ML3404 and SP600125. The present study indicated that PRDX6 overexpression inactivated p38 MAPK and JNK pathway through decrease AngII-induced inflammation, oxidative stress and endothelial dysfunction leading to attenuation of endothelial cell damage.

Inhibitation of cellular toxicity of gold nanoparticles by surface encapsulation of silica shell for hepatocarcinoma cell application.

Nanotechnology, as a double-edged sword, endows gold nanoparticles (GNPs) more "power" in bioimaging and theragnostics, whereas an outstanding issue associated with the biocompatibility of GNPs should also be addressed. Especially for the silica-coated gold nanospheres (GNSs) and gold nanorods (GNRs), there is increasing attention to explore the application, because the surface silica encapsulation has been proved to be an alternative strategy for other organic surface coatings. However, among those reports there are very limited publications to focus on the toxicity of silica-coated GNSs and GNRs. Besides, the existing detoxification methods via surface chemistry on GNPs greatly improve the biocompatibility but still undergo challenges for high dose (>100 pM) demand and long-term stability. Here, we demonstrated a straightforward, low-cost, universal strategy for the surface chemistry on GNPs via silica encapsulating. Different size, shape, dose, and surface capping of GNPs for the nanotoxicity test have been carefully discussed. After silica encapsulating, the detoxification for all GNPs presents significantly from HepG2 cell proliferation results, especially for the GNRs. This new straightforward strategy will definitely rationalize the biocompatibility issue of GNPs and also provide potential for other surface chemistry methodology in biomedical fields.