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Discovery of 2(1)-Quinoxalinone Derivatives as Potent and Selective MAT2A Inhibitors for the Treatment of MTAP-Deficient Cancers.
J Med Chem
January 2025
Department of Pharmaceutical Engineering, School of Engineering, China Pharmaceutical University, 639 Longmian Avenue, Nanjing 211198, China.
Methionine adenosyltransferase 2A (MAT2A) has emerged as a synthetic lethal drug target in cancers bearing homozygous methylthioadenosine phosphorylase (MTAP) gene deletion. Despite the remarkable progress in the discovery and development of MAT2A inhibitors, current understanding about the selectivity of these compounds toward MTAP-deficient cancers is relatively limited. To improve the selectivity of MAT2A inhibitors for MTAP-deficient cancers remains a significant challenge.
View Article and Find Full Text PDFD-ribose-5-phosphate inactivates YAP and functions as a metabolic checkpoint.
J Hematol Oncol
January 2025
Department of Radiation Oncology, Henan Provincial Key Laboratory of Radiation Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, People's Republic of China.
Background: Targeting glucose uptake by glucose transporter (GLUT) inhibitors is a therapeutic opportunity, but efforts on GLUT inhibitors have not been successful in the clinic and the underlying mechanism remains unclear. We aim to identify the key metabolic changes responsible for cancer cell survival from glucose limitation and elucidate its mechanism.
Methods: The level of phosphorylated YAP was analyzed with Western blotting and Phos-tag immunoblotting.
Renal impairment as a risk factor for chemotherapy induced neutropenia in the treatment of trifluridine/thymidine phosphorylase inhibitor plus bevacizumab.
Sci Rep
January 2025
Department of Gastroenterological Surgery, Osaka Metropolitan University Graduate School of Medicine, 1-4-3 Asahi-machi Abeno-ku, Osaka City, 545-8585, Osaka Prefecture, Japan.
Although the phase III SUNLIGHT trial has demonstrated the survival benefit of the addition of bevacizumab (Bmab) to trifluridine/thymidine phosphorylase inhibitor (FTD/TPI), neutropenia, which frequently occurs during FDT/TPI + Bmab therapy, is a concern for clinicians. As TPI is excreted by the kidneys, the risk of adverse events is likely to be high in patients with an impaired renal function. This study aimed to investigate the relationship between renal impairment and the incidence of chemotherapy-induced neutropenia during FTD/TPI + Bmab therapy using real-world data.
View Article and Find Full Text PDFThymidine Phosphorylase Promotes Abdominal Aortic Aneurysm via VSMC Modulation and Matrix Remodeling in Mice and Humans.
Cardiovasc Ther
January 2025
Department of Biomedical Sciences, Joan C. Edwards School of Medicine at Marshall University, Huntington, West Virginia, USA.
Thymidine phosphorylase (TYMP) promotes platelet activation and thrombosis while suppressing vascular smooth muscle cell (VSMC) proliferation. Both processes are central to the development and progression of abdominal aortic aneurysms (AAAs). We hypothesize that TYMP plays a role in AAA development.
View Article and Find Full Text PDFNesfatin-1 as a crucial mediator of glucose homeostasis in the reptile, Hemidactylus flaviviridis.
Sci Rep
December 2024
University of Jammu, Jammu and Kashmir, 180006, India.
Nesfatin-1 is a crucial regulator of energy homeostasis in mammals and fishes, however, its metabolic role remains completely unexplored in amphibians, reptiles, and birds. Therefore, present study elucidates role of nesfatin-1 in glucose homeostasis in wall lizard wherein fasting stimulated hepatic nucb2/nesfatin-1, glycogen phosphorylase (glyp), phosphoenolpyruvate carboxykinase (pepck), and fructose 1,6-bisphosphatase (fbp), while feeding upregulated pancreatic nucb2/nesfatin-1 and insulin, suggesting towards tissue-specific dual role of nesfatin-1 in glucoregulation. The glycogenolytic/gluconeogenic role of nesfatin-1 was further confirmed by an increase in media glucose levels along with heightened hepatic pepck and fbp expression and concomitant decline in liver glycogen content in nesfatin-1-treated liver of wall lizard.
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