Repression of YEATS2 induces cellular senescence in hepatocellular carcinoma and inhibits tumor growth.

Hepatocellular carcinoma (HCC) stands as the third leading cause of cancer-related fatalities globally. In this study, we observed a significant increase in the expression level of the gene in HCC patients, and it is negatively correlated with the patients' survival rate. While we have previously identified the association between YEATS2 and the survival of pancreatic cancer cells, the regulatory mechanisms and significance in HCC are still to be fully elucidated.

ARF6 promotes hepatocellular carcinoma proliferation through activating STAT3 signaling.

Background: Hepatocellular Carcinoma (HCC) possesses the high mortality in cancers worldwide. Nevertheless, the concrete mechanism underlying HCC proliferation remains obscure. In this study, we show that high expression of ARF6 is associated with a poor clinical prognosis, which could boost the proliferation of HCC.

DDR1 promotes hepatocellular carcinoma metastasis through recruiting PSD4 to ARF6.

Discoidin domain receptor 1 (DDR1) is a member of the receptor tyrosine kinase family, and its ligand is collagen. Previous studies demonstrated that DDR1 is highly expressed in many tumors. However, its role in hepatocellular carcinoma (HCC) remains obscure.

The APC/C Complex Coordinates With OMA-1 to Regulate the Oocyte-to-Embryo Transition in .

During oocyte maturation and the oocyte-to-embryo transition, key developmental regulators such as RNA-binding proteins coordinate translation of particular messenger RNA (mRNAs) and related developmental processes by binding to their cognate maternal mRNAs. In the nematode , these processes are regulated by a set of CCCH zinc finger proteins. Oocyte maturation defective-1 (OMA-1) and OMA-2 are two functionally redundant CCCH zinc finger proteins that turnover rapidly during the first embryonic cell division.

ERAD deficiency promotes mitochondrial dysfunction and transcriptional rewiring in human hepatic cells.

Mitochondrial dysfunction is associated with a variety of human diseases including neurodegeneration, diabetes, nonalcohol fatty liver disease (NAFLD), and cancer, but its underlying causes are incompletely understood. Using the human hepatic cell line HepG2 as a model, we show here that endoplasmic reticulum-associated degradation (ERAD), an ER protein quality control process, is critically required for mitochondrial function in mammalian cells. Pharmacological inhibition or genetic ablation of key proteins involved in ERAD increased cell death under both basal conditions and in response to proinflammatory cytokines, a situation frequently found in NAFLD.

The Dynamics of P Granule Liquid Droplets Are Regulated by the Germline RNA Helicase GLH-1 via Its ATP Hydrolysis Cycle.

P granules are phase-separated liquid droplets that play important roles in the maintenance of germ cell fate in Both the localization and formation of P granules are highly dynamic, but mechanisms that regulate such processes remain poorly understood. Here, we show evidence that the VASA-like germline RNA helicase GLH-1 couples distinct steps of its ATPase hydrolysis cycle to control the formation and disassembly of P granules. In addition, we found that the phenylalanine-glycine-glycine repeats in GLH-1 promote its localization at the perinucleus.

Endoplasmic Reticulum-Associated Degradation (ERAD) Has a Critical Role in Supporting Glucose-Stimulated Insulin Secretion in Pancreatic β-Cells.

The molecular underpinnings of β-cell dysfunction and death leading to diabetes are not fully elucidated. The objective of the current study was to investigate the role of endoplasmic reticulum-associated degradation (ERAD) in pancreatic β-cells. Chemically induced ERAD deficiency in the rat insulinoma cell line INS-1 markedly reduced glucose-stimulated insulin secretion (GSIS).

Whole-body aerosol exposure of cadmium chloride (CdCl2) and tetrabromobisphenol A (TBBPA) induced hepatic changes in CD-1 male mice.

Cadmium (Cd) and tetrabromobisphenol A (TBBPA) are two prevalent contaminants in e-waste recycling facilities. However, the potential adversely health effect of co-exposure to these two types of pollutants in an occupational setting is unknown. In this study, we investigated co-exposure of these two pollutants on hepatic toxicity in CD-1 male mice through a whole-body aerosol inhalation route.

Daily intake of polybrominated diphenyl ethers via dust and diet from an e-waste recycling area in China.

This study was designed to estimate the human risk to polybrominated diphenyl ethers (PBDEs) exposure via two main exposure routes (dust and diet) in an e-waste recycling area in southern China. A total of 134 dust samples and 129 food samples were analyzed by gas chromatography/mass spectrometry (GC/MS). The mean concentration of ΣPBDE in in-house dust (38,685ng/g dw) was higher than that in out-house dust (24,595ng/g).