Environmental Toxicology最新文献

RETRACTION: L. Daren, Y. Dan, W. Jinhong, and L. Chao, “NIK-Mediated Reactivation of SIX2 Enhanced the CSC-like Traits of Hepatocellular Carcinoma Cells Through Suppressing Ubiquitin–Proteasome System,” Environmental Toxicology 39, no. 2 (2024): 583-591, https://doi.org/10.1002/tox.23892.

The above article, published online on 17 July 2023, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Christyn Bailey; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted.

Methylmercury (MeHg) is markedly toxic to humans. Our study explores whether MeHg and high-fat diet (HFD) can impair the intestinal barrier with microbiota dysbiosis in mice. Weanling mice were fed to HFD or standard diet for 40 days. In the last 20 days of diets, mice received either MeHg (20 mg/L) or drinking water. Proximal small intestine, cecum, and hair samples were collected. Villus length, crypt depth, villus/crypt length, mucin2 and lysozyme-positive cell counts, ZO-1 and occludin gene expression, and intestinal functional permeability were analyzed to assess the intestinal barrier. Blood samples were drawn to assess lipid parameters. Gut microbiome profiling was conducted with DNA from fecal/cecal samples. In addition, we analyzed ZO-1 immunofluorescence in the colon and small intestine. HFD increased MDA, Mucin2, and reduced villus height, crypt depth, villus/crypt length, lysozyme(+)-cell count, and increased intestinal permeability, regardless of MeHg intoxication. MeHg-HFD combination affected the intestinal barrier, decreasing ZO-1, occludin, and Nrf2 transcription, and increased permeability. HFD increased total plasma cholesterol and triglycerides. Only MeHg-HFD reduced microbiome alpha-diversity along with colonic ZO-1 immunolabeling loss compared to non-intoxicated mice fed a control diet. Regardless of diet, the genera Streptococcus, Psychrobacter, Facklamia, and Corynebacterium were severely depleted following MeHg intoxication. Other groups, such as Atopostipes and Jeotgalicoccus, were not altered by MeHg or HFD alone, but were significantly reduced by the combined HFD-MeHg. Synergistic effects of MeHg-HFD on the mucosa-associated microbiota are more pronounced than their individual effects. Our findings suggest that MeHg intoxication does not cause extensive dysbiosis but led to intestinal barrier disruption.

Carcinomatosis is one of the leading threats to human public fitness. HNF1B is a critical transcription element in vertebrate proliferation and oncogenesis, which has been shown to play roles in reactive oxygen species (ROS) metabolism. Our previous results have identified HNF1B as a tumor suppressor that could inhibit the malignant progression of prostate cancer. Yet there is no pan-carcinomatosis analysis of HNF1B, which could help us better understand common and unique underlying mechanisms in mankind knubs to enhance novel and competent treatment. Here, in our research, we evaluated the utterance pattern and explored the function of HNF1B in 33 knub categories using the data from the Cancer Genome Atlas Program (TCGA), Gene Expression Omnibus (GEO), and CLNICAL PROTEOMICTUMOR ANALYSIS CONSORTIUM (CPTAC) dataset. We found different HNF1B roles in various cancer types. HNF1B was upregulated in CHOL, STAD, KIRP, and THCA, and was downregulated in GBM, KICH, COAD, KIRC, LUSC, SARC, PAAD, and TGCT. Prognostic analyses indicated that higher HNF1B displayed better illness outcomes in BLCA, READ, and PRAD, while poorer outcomes in LUSC and THYM. HNF1B mutation was most frequent in endometrial cancer but was not associated with disease prognosis. It was discovered that HNF1B utterance relevant to endothelial cell penetration status in BLCA, ESCA, LUAD, LUSC, and TGCT, and carcinomatosis-associated fibroblast infiltration was observed in ESCA, KIRC, LIHC, and TGCT. Moreover, functional enrichment analysis disclosed that metabolism-related functions were implicated in the function of HNF1B. Taken together, our pan- carcinomatosis analysis showed the complicated roles of HNF1B in a variety of carcinomatoses, being able to improve the extensive comprehension of HNF1B's role in tumorigenesis.