In this study, our findings indicated that FOXO1 expression frequently decreased in glioma tissues and cells. FOXO1 expression decrease correlated with glioma progression and predicted a worse overall survival of glioma patients. Restored FOXO1 expression inhibited glioma cells invasion and suppressed glioma cells proliferation in vitro and growth in vivo. Additionally, we found that KLF4 expression frequently increased in glioma tissues and negatively correlated with FOXO1 expression. Bioinformatics analysis and experimental results indicated that KLF4 transcriptionally repressed FOXO1 expression in glioma cells. Moreover, KLF4 expression increase correlated with glioma progression and predicted a poorer overall survival of glioma patients. KLF4 knockdown attenuated glioma cells invasion and growth. These data provide a rationale for targeted intervention on KLF4-FOXO1 signaling pathway to suppress glioma progression.
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http://dx.doi.org/10.18632/oncotarget.13184 | DOI Listing |
Environ Pollut
January 2025
Department of Toxicology, School of Public Health, Hebei Medical University, Shijiazhuang, 050017, PR China; Hebei Key Laboratory of Environment and Human Health, Hebei Province, Shijiazhuang, 050017, PR China. Electronic address:
Perfluorooctane sulfonate (PFOS), a prevalent perfluoroalkyl substance (PFAS), is widely present in various environmental media, animals, and even human bodies. It primarily accumulates in the liver, contributing to the disruption of hepatic metabolic homeostasis. However, the precise mechanism underlying PFOS-induced hepatic glucolipid metabolic disorders remains elusive.
View Article and Find Full Text PDFJ Chromatogr B Analyt Technol Biomed Life Sci
December 2024
The College of Life Sciences, Northwest University, Xi'an, China. Electronic address:
Zhi Bai Heye Fang (AR-PCC-NF) exerts a positive effect on glycolipid metabolic disorders in the clinical setting; however, its efficacy components and mechanisms of action remain unclear. Glycolipid metabolic disorders in mice were used to evaluate the therapeutic effects of AR-PCC-NF and its individual components, and the chemical components of AR-PCC-NF were detected by HPLC. An insulin-resistant cell model was then treated with 12 biological components in vitro, and seven candidate active components were administered to mice with glycolipid metabolic disorders to investigate the efficacy and mechanism of AR-PCC-NF.
View Article and Find Full Text PDFShock
December 2024
Department of Emergency Medicine, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan 430074, China.
Aims: Brain injury occupies the predominant cause of neurological dysfunction and mortality after successful cardiopulmonary resuscitation (CPR) from cardiac arrest (CA). This study investigates the role and mechanism of Sirtuin 6 (SIRT6) in post-cardiac arrest brain injury in rats.
Methods: All rats were subjected to asphyxial CA followed by CPR.
Front Immunol
January 2025
Department of Medical Microbiology and Nanobiomedical Engineering, Medical University of Białystok, Białystok, Poland.
Acne vulgaris (AV) is a chronic inflammatory condition of the pilosebaceous units characterized by multiple immunologic, metabolic, hormonal, genetic, psycho-emotional dysfunctions, and skin microbiota dysbiosis. The latter is manifested by a decreased population (phylotypes, i.e.
View Article and Find Full Text PDFBMC Pharmacol Toxicol
December 2024
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.
Background: UpToDate, no drugs have been approved to treat nonalcoholic steatohepatitis, the advanced stage of the most prevalent liver disease, non-alcoholic fatty liver disease. The present study was conducted to explore the potential influences of L-carnitine on the pathomechanisms of hepatic injury that mediate progression to non-alcoholic steatohepatitis in dexamethasone-toxified rats.
Methods: Male Wistar rats were allocated as follows: dexamethasone group, rats received dexamethasone (8 mg/kg/day, intraperitoneally) for 6 days; DEXA-LCAR300, DEXA-LCAR500, and DEXA-MET groups, rats administered L-carnitine (300 or 500 mg/kg/day, IP) or metformin (500 mg/kg/day, orally) one week prior to dexamethasone injection (8 mg/kg/day, IP) and other six days alongside dexamethasone administration.
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