Triggering Oxygen Redox Cycles in Nickel Ferrite by Octahedral Geometry Engineering for Enhancing Oxygen Evolution.

Spinel-type nickel ferrite (NiFeO, x≤1) is a widely used electrocatalyst for the oxygen evolution reaction (OER). Due to the lower hybridization of metal-d and oxygen-p orbitals, the OER process on NiFeO follows the sluggish adsorbate evolution mechanism (AEM). Generally, activating the lattice oxygen to trigger the lattice-oxygen-mediated mechanism (LOM) can enhance the OER activity.

GPX2 predicts recurrence-free survival and triggers the Wnt/β-catenin/EMT pathway in prostate cancer.

Objective: This study aimed to establish a prognostic model related to prostate cancer (PCa) recurrence-free survival (RFS) and identify biomarkers.

Methods: The RFS prognostic model and key genes associated with PCa were established using Least Absolute Shrinkage and Selection Operator (LASSO) and Cox regression from the Cancer Genome Atlas (TCGA)-PRAD and the Gene Expression Omnibus (GEO) GSE46602 datasets. The weighted gene co-expression network (WGCNA) was used to analyze the obtained key modules and genes, and gene set enrichment analysis (GSEA) was performed.

Protective Effect of Melatonin for Renal Ischemia-Reperfusion Injury: A Systematic Review and Meta-Analysis.

Renal ischemia-reperfusion (I/R) injury is one of the major causes related to acute kidney damage. Melatonin has been shown as a powerful antioxidant, with many animal experiments have been designed to evaluate the therapeutic effect of it to renal I/R injury. This systematic review aimed to assess the therapeutic effect of melatonin for renal I/R injury in animal models.

STAT3-regulated LncRNA LINC00160 mediates cell proliferation and cell metabolism of prostate cancer cells by repressing RCAN1 expression.

Long non-coding RNA (LncRNA) LINC00160 was reported to be associated with cancer progression and mediates drug resistance. However, the role of LINC00160 in prostate cancer remains unclear. The study sought to study the function of LINC00160 in prostate cancer.

Neuronal calcitonin gene-related peptide promotes prostate tumor growth in the bone microenvironment.

Advanced stage of prostate cancer cells preferentially metastasizes to varying bones of prostate cancer patients, resulting in incurable disease with poor prognosis and limited therapeutical treatment options. Calcitonin gene-related peptide (CGRP), a neuropeptide produced by prostate gland, is known to play a pivotal role in facilitating tumor growth and metastasis of numerous human cancers. In this study, we aim to investigate the clinical relevance of CGRP in prostate cancer patients and the effects of CGRP and CGRP antagonists on prostate tumor growth in the mouse model.

Bisdemethoxycurcumin in combination with α-PD-L1 antibody boosts immune response against bladder cancer.

Curcumin was recently discovered to strengthen immune response through multiple mechanisms. Cytotoxic CD8 T-cells play a critical role in modulating anticancer immune response, but is severely restricted by T-cell exhaustion. Bladder carcinomas express PD-L1 and can abrogate CD8 T-cell response.

MicroRNA-218 inhibits tumor growth and increases chemosensitivity to CDDP treatment by targeting BCAT1 in prostate cancer.

MicroRNAs have been reported to be associated with chemosensitivity of several types of cancers. However, the underlying molecular mechanisms are poorly understood. In this study, we explored miR-218 increased the chemosensitivity to cis-diaminedichloroplatinum treatment of prostate cancer.

Asparaginyl endopeptidase promotes proliferation and invasiveness of prostate cancer cells via PI3K/AKT signaling pathway.

Recurrence and metastasis are the major lethal causes of prostate cancer. It is urgent to find out the mechanisms and key factors governing prostate cancer progression and metastasis for developing new therapeutic strategies. Asparaginyl endopeptidase (AEP) overexpression has been found in a number of solid tumors.

Effect of PI3K/Akt Signaling Pathway on the Process of Prostate Cancer Metastasis to Bone.

We sought to study the effects of PI3K/Akt pathway and its downstream substrate NF-κB on prostate cancer bone metastatic process. Expression level of active p-Akt in PC3 cells was upregulated by transient expression with constitutively active plasmid CA-Akt or, alternatively, suppressed by dominant negative construct DN-Akt. NF-κB activity was determined by luciferase reporter assays.