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PTPN23-dependent activation of PI3KC2α is a therapeutic vulnerability of BRAF-mutant cancers.
J Exp Med
March 2025
Institute of Cancer Research, Shenzhen Bay Laboratory , Shenzhen, China.
BRAF mutations drive initiation and progression of various tumors. While BRAF inhibitors are effective in BRAF-mutant melanoma patients, intrinsic or acquired resistance to these therapies is common. Here, we identify non-receptor-type protein tyrosine phosphatase 23 (PTPN23) as an alternative effective target in BRAF-mutant cancer cells.
View Article and Find Full Text PDFDiscovery of noncovalent diaminopyrimidine-based Inhibitors for glioblastoma via a dual FAK/DNA targeting strategy.
Eur J Med Chem
January 2025
School of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China. Electronic address:
Temozolomide, a widely used alkylating agent for glioblastoma treatment, faces significant challenges due to the development of resistance, which severely impacts patient survival. This underscores the urgent need for novel strategies to overcome this barrier. Focal adhesion kinase (FAK), an intracellular non-receptor tyrosine kinase, is highly expressed in glioblastoma cells and has been identified as a promising therapeutic target for anti-glioblastoma drug development.
View Article and Find Full Text PDFPD-L1 monoclonal antibody alleviated MI injury of left ventricular function via modulating CD47/SHP2/SIRPα/SYK/FcγR signalings in tumor associated macrophages.
Sci Rep
January 2025
Department of Radiotherapy, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
To investigate how PD-L1 monoclonal antibodies (mAbs) affect the left ventricular function in mice with myocardial infarction (MI) and through what mechanisms they exert their effects. In vivo experiments were conducted using 27 female BALB/c mice, which were divided equally into 3 groups. Cardiac function was assessed by ultrasound.
View Article and Find Full Text PDFJiangzhi Granule Ameliorates JNK-Mediated Mitochondrial Dysfunction to Reduce Lipotoxic Liver Injury in NASH.
Diabetes Metab Syndr Obes
January 2025
Institute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Purpose: Mitochondrial dysfunction mediated by c-Jun N-terminal kinase (JNK) plays an important role in lipotoxic liver injury in nonalcoholic steatohepatitis (NASH). This study aims to investigate the pharmacological mechanism of Jiangzhi Granule (JZG), a Chinese herbal formula against NASH, with a focus on its regulation of JNK signaling-mediated mitochondrial function.
Methods: Hepatocytes were induced by palmitic acid (PA) for 24 h to establish an in vitro lipotoxic model, which was simultaneously treated with either JZG or vehicle control.
Study on SHP2 Conformational Transition and Structural Characterization of Its High-Potency Allosteric Inhibitors by Molecular Dynamics Simulations Combined with Machine Learning.
Molecules
December 2024
School of Chemical Sciences, University of Chinese Academy of Sciences, No. 19A, Yuquan Road, Beijing 100049, China.
The src-homology 2 domain-containing phosphatase 2 (SHP2) is a human cytoplasmic protein tyrosine phosphatase that plays a crucial role in cellular signal transduction. Aberrant activation and mutations of SHP2 are associated with tumor growth and immune suppression, thus making it a potential target for cancer therapy. Initially, researchers sought to develop inhibitors targeting SHP2's catalytic site (protein tyrosine phosphatase domain, PTP).
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