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Iridin is a natural flavonoid found in documented for its broad spectrum of biological activities like antioxidant, antitumor, and antiproliferative effects. In the present study, we have investigated the antitumor potential of iridin in AGS gastric cancer cells. Iridin treatment decreases AGS cell growth and promotes G2/M phase cell cycle arrest by attenuating the expression of Cdc25C, CDK1, and Cyclin B1 proteins. Iridin-treatment also triggered apoptotic cell death in AGS cells, which was verified by cleaved Caspase-3 (Cl- Caspase-3) and poly ADP-ribose polymerase (PARP) protein expression. Further apoptotic cell death was confirmed by increased apoptotic cell death fraction shown in allophycocyanin (APC)/Annexin V and propidium iodide staining. Iridin also increased the expression of extrinsic apoptotic pathway proteins like Fas, FasL, and cleaved Caspase-8 in AGS cells. On the contrary, iridin-treated AGS cells did not show variations in proteins related to an intrinsic apoptotic pathway such as Bax and Bcl-xL. Besides, Iridin showed inhibition of PI3K/AKT signaling pathways by downregulation of (p-PI3K, p-AKT) proteins in AGS cells. In conclusion, these data suggest that iridin has anticancer potential by inhibiting PI3K/AKT pathway. It could be a basis for further drug design in gastric cancer treatment.
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http://dx.doi.org/10.3390/molecules26092802 | DOI Listing |
Heart Rhythm
September 2025
Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, United States. Electronic address:
Background: Electronic nicotine delivery systems (ENDS) utilize "E-liquids" in order to generate "E-vapor", an inhalable aerosolized mixture containing nicotine and flavors. Flavored ENDS are very popular among teens who vape, however, the possible cardiac electrophysiological harm of inhalation exposure to flavored ENDS are not fully understood.
Objective: To test if inhalation exposure to flavoring carbonyls in e-liquids compromises mitochondrial integrity, increases oxidative stress, and leads to cardiac electrophysiological toxicity.
Cell Signal
September 2025
Department of Obstetrics and Gynecology, the First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei 230022, Anhui, China; NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract (Anhui Medical University), No. 81 Meishan Road, Hefei 230032, Anhui, China; Engin
Leber's hereditary optic neuropathy (LHON), a mitochondrial disorder marked by central vision loss, exhibits incomplete penetrance and male predominance. Since there are no adequate models for understanding the rapid vision loss associated with LHON, we generated induced pluripotent stem cells (iPSCs) from LHON patients carrying the pathogenic m.3635G > A mutation and differentiated them into retinal pigment epithelium (RPE) cells.
View Article and Find Full Text PDFChem Biol Interact
September 2025
School of Pharmacy, Hubei University of Chinese Medicine, Wuhan, 430065, People's Republic of China; Hubei Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine, Wuhan, 430065, People's Republic of China; Hubei Shizhen Laboratory, Wuhan,430061, People 's
Intrahepatic cholangiocarcinoma (iCCA) is a malignant liver tumor with insidious onset, limited treatments, and poor prognosis. Recent studies show celecoxib exerts marked cytotoxic effects on cholangiocarcinoma cell lines, suggesting its potential as an iCCA therapy. However, the potential molecular and cellular mechanisms that link celecoxib treatment to its toxicological outcomes remain unclear.
View Article and Find Full Text PDFExp Neurol
September 2025
Department of Human Genetics, Emory University School of Medicine, Atlanta, GA, USA. Electronic address:
Synapse refinement through the elimination of excess synapses is crucial for proper neuronal circuitry during development and adulthood, and the phagocytic activity of astrocytes plays an important role in this process. Failure to remove excess synapses can lead to neurological and neurodevelopmental disorders like epilepsy and autism spectrum disorder (ASD). The adhesion G protein-coupled receptor BAI1/ADGRB1 contributes to phagocytosis in various tissues, including the clearance of apoptotic myoblasts in skeletal muscle and epithelial cells in the intestine.
View Article and Find Full Text PDFJ Biol Chem
September 2025
Department of Biology, Stanford University, Stanford, CA 94305, USA. Electronic address:
Small molecules serve as valuable tools for probing non-apoptotic cell death mechanisms. The small molecule caspase independent lethal 56 (CIL56) induces a unique form of non-apoptotic cancer cell death that is promoted by a complex formed between zDHHC palmitoyltransferase 5 (ZDHHC5) and an accessory protein, golgin A7 (GOLGA7, also known as GCP16). The structure and function of this complex in non-apoptotic cell death regulation remain poorly understood.
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