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Brd4 modulates metabolic endotoxemia-induced inflammation by regulating colonic macrophage infiltration in high-fat diet-fed mice.
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Fujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, Institute for Basic Medical Sciences, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
High-fat diet (HFD) induces low-grade chronic inflammation, contributing to obesity and insulin resistance. However, the precise mechanisms triggering obesity-associated metabolic inflammation remain elusive. In this study, we identified epigenetic factor Brd4 as a key player in this process by regulating the expression of Ccr2/Ccr5 in colonic macrophage.
View Article and Find Full Text PDFEGCG activates Keap1/P62/Nrf2 pathway, inhibits iron deposition and apoptosis in rats with cerebral hemorrhage.
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Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, China.
Intracerebral hemorrhage (ICH) is a common cerebrovascular disease characterized by a high incidence, disability rate, and mortality. Epigallocatechin gallate (EGCG), a key catechin compound found in green tea, has received increasing attention for its potential neuroprotective and therapeutic effects in neurological disorders. Studies have indicated that EGCG may influence various signaling pathways and molecular targets, including the inhibition of oxidative stress, reduction of inflammatory responses, suppression of cell apoptosis, regulation of cell survival, and enhancement of autophagy.
View Article and Find Full Text PDFS100A4 contributes to colorectal carcinoma aggressive behavior and to chemoradiotherapy resistance in locally advanced rectal carcinoma.
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Department of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-ku, Sagamihara, 252-0374, Kanagawa, Japan.
To investigate the functional role of S100A4 in advanced colorectal carcinoma (Ad-CRC) and locally advanced rectal carcinoma (LAd-RC) receiving neoadjuvant chemoradiotherapy (NCRT). We analyzed histopathological and immunohistochemical sections from 150 patients with Ad-CRC and 177 LAd-RC patients treated with NCRT. S100A4 knockout (KO) HCT116 cells were also used.
View Article and Find Full Text PDFNovel anoikis-related diagnostic biomarkers for aortic dissection based on machine learning.
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Department of Dermatology, Hunan Key Laboratory of Skin Cancer and Psoriasis, Hunan Engineering Research Center of Skin Health and Disease, Xiangya Clinical Research Center for Cancer Immunotherapy, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, China.
Aortic dissection (AD) is one of the most dangerous diseases of the cardiovascular system, which is characterized by acute onset and poor prognosis, while the pathogenesis of AD is still unclear and may affect or even delay the diagnosis of AD. Anchorage-dependent cell death (Anoikis) is a special mode of cell death, which is programmed cell death caused by normal cells after detachment from extracellular matrix (ECM) and has been widely studied in the field of oncology in recent years. In this study, we applied bioinformatics analysis, according to the results of research analysis and Gene Ontology (GO), as well as Kyoto Encyclopedia of Genes and Genomes (KEGG), finally found 3 anoikis-related genes (ARGs) based on machine learning.
View Article and Find Full Text PDFEfficacy of glutathione inhibitor eprenetapopt against the vulnerability of glutathione metabolism in SMARCA4-, SMARCB1- and PBRM1-deficient cancer cells.
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Division of Cancer Therapeutics, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Mutation of genes related to the SWI/SNF chromatin remodeling complex is detected in 20% of all cancers. The SWI/SNF chromatin remodeling complex comprises about 15 subunits and is classified into three subcomplexes: cBAF, PBAF, and ncBAF. Previously, we showed that ovarian clear cell carcinoma cells deficient in ARID1A, a subunit of the cBAF complex, are synthetic lethal with several genes required for glutathione (GSH) synthesis and are therefore sensitive to the GSH inhibitor eprenetapopt (APR-246).
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