Willin/ has been reported as a potential Alzheimer's disease (AD) risk gene in a series of genome-wide association and neuroimaging studies; however, the mechanisms underlying its potential role in AD pathogenesis remain unknown. Here, we demonstrate the direct effects of Aβ on Willin/FRMD6 expression and position mitochondrial oxidative stress as a novel potential mechanism underlying the role of Willin/FRMD6 in AD pathogenesis. Specifically, using mouse hippocampal HT-22 cells and primary mouse neurons, we show that Aβ induces downregulation of Willin/FRMD6 protein expression.
View Article and Find Full Text PDFBMC Pharmacol Toxicol
April 2022
Background: The main causes of lung cancer are smoking, environmental pollution and genetic susceptibility. It is an indisputable fact that PAHs are related to lung cancer, and benzo(a) pyrene is a representative of PAHs. The purpose of the current investigation was to investigate the interaction between AhR and HIF-1 signaling pathways in A549 cells, which provide some experimental basis for scientists to find drugs that block AhR and HIF-1 signaling pathway to prevent and treat cancer.
View Article and Find Full Text PDFThe FERM domain-containing protein 6 (FRMD6), also known as Willin, is an upstream regulator of Hippo signaling that has recently been shown to modulate actin cytoskeleton dynamics and mechanical phenotype of neuronal cells through ERK signaling. Physiological functions of Willin/FRMD6 in the nervous system include neuronal differentiation, myelination, nerve injury repair, and vesicle exocytosis. The newly established neuronal role of Willin/FRMD6 is of particular interest given the mounting evidence suggesting a role for Willin/FRMD6 in Alzheimer's disease (AD), including a series of genome wide association studies that position Willin/FRMD6 as a novel AD risk gene.
View Article and Find Full Text PDFWillin/FRMD6 is part of a family of proteins with a 4.1 ezrin-radixin-moesin (FERM) domain. It has been identified as an upstream activator of the Hippo pathway and, when aberrant in its expression, is associated with human diseases and disorders.
View Article and Find Full Text PDFPurpose: To explore associations of CYP2E1 and NAT2 polymorphisms with lung cancer susceptibility among Mongolian and Han populations in the Inner Mongolian region.
Materials And Methods: CYP2E1 and NAT2 polymorphisms were detected by PCR-RFLP in 930 lung cancer patients and 1000 controls.
Results: (1) Disequilibrium of the distribution of NAT2 polymorphism was found in lung cancer patients among Han and Mongolian populations (p=0.
Background: +936C>T polymorphism of vascular endothelial growth factor (VEGF) is one of the most investigated polymorphisms, it has been suggested that it plays a vital role in tumorigenesis. Intensive studies centering on the association between VEGF +936C>T polymorphism and lung cancer risk or lung cancer patients' overall survival were conducted in recent years, but with inconclusive and ambiguous results.
Objective And Methods: We investigated whether VEGF +936C>T polymorphism influences lung cancer risk and lung cancer patients' overall survival (OS) using pooled odds ratios (ORs) and hazard ratios (HRs) with their corresponding 95% confidence intervals (CI) under different genetic models.