Glesatinib, a c-MET/SMO Dual Inhibitor, Antagonizes P-glycoprotein Mediated Multidrug Resistance in Cancer Cells
Glesatinib, a c-MET/SMO Dual Inhibitor, Antagonizes P-glycoprotein Mediated Multidrug Resistance in Cancer Cells Qingbin Cui1,2, Chao-Yun Cai2, Hai-Ling Gao2,3, Liang Ren1, Ning Ji2,4, Pranav Gupta2, Yuqi Yang2, Suneet Shukla5, Suresh V. Ambudkar5, Dong-Hua Yang2 and Zhe-Sheng Chen2* 1School of Public Health, Guangzhou Medical University, Guangdong, China 2Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, United States 3Department of Histology and Embryology, Clinical Medical College, Weifang Medical University, Weifang, China 4Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin, China 5Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, United States Multidrug resistance (MDR) is one of the leading causes of treatment failure in cancer chemotherapy. One major mechanism of MDR is the overexpressing of ABC transporters, whose inhibitors hold promising potential in antagonizing MDR. Glesatinib is a dual inhibitor of c-Met and SMO that is under phase II clinical trial for non-small cell lung cancer. In this work, we report the reversal effects of glesatinib to P-glycoprotein (P-gp) mediated MDR. Glesatinib can sensitize paclitaxel, doxorubicin, colchicine resistance to P-gp overexpressing KB-C2, SW620/Ad300, and P-gp transfected Hek293/ABCB1...
ConclusionsThese results demonstrate that a novel proton-coupled organic cation antiporter plays a predominant role in the blood to brain influx of AC, MA and HA at the BBB, and thus affect the safety of Aconitum species.Graphical abstract
This study investigated the cardioprotective effect of vitexin against MIRI and its possible mechanism. Isolated SD rat hearts were subjected to MIRI in a Langendorff perfusion system, and H9c2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro. Ex vivo experiments showed improved left ventricular function and reduced infarct size in the vitexin group. Transmission electron microscopy showed that I/R caused outer mitochondrial membrane rupture, cristae disappearance and vacuolation, while vitexin reduced mitochondrial damage and ultimately reduced cardiomyocyte apoptosis. In vitro, vitexin protected H9c2 cells fr...
ConclusionsOur study demonstrates the antitumor effect of IL-24 on endometrial cancer and shows that IL-24 may be a promising therapeutic gene for endometrial cancer gene therapy.Graphical abstract
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