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• W2894930796 abstract "Abstract Membrane type‐1 matrix metalloproteinase ( MT 1‐ MMP ) possesses both extracellular proteolytic and intracellular signal‐transducing functions in tumorigenesis. An imbalance in MT 1‐ MMP expression and/or function triggers a metastatic, invasive, and therapy resistance phenotype. MT 1‐ MMP is involved in extracellular matrix ( ECM ) proteolysis, activation of latent MMP s, as well as in autophagy signaling in human hepatoma and glioblastoma cells. A low autophagy index in tumorigenesis has been inferred by recent studies where autophagic capacity was decreased during tumor progression. Here, we establish ARP 101 as a dual‐function small‐molecule inhibitor against MT 1‐ MMP ECM hydrolysis and autophagy signal‐transducing functions in a model of grade IV glioblastoma cells. ARP 101 inhibited concanavalin‐A‐mediated pro MMP ‐2 activation into MMP ‐2, as well as MT 1‐ MMP auto‐proteolytic processing. When overexpressing recombinant Wt MT 1‐ MMP , ARP 101 inhibited pro MMP ‐2 activation and triggered the formation of MT 1‐ MMP oligomers that required trafficking to the plasma membrane. ARP 101 further induced cell autophagy as reflected by increased formation of acidic vacuole organelles, LC 3 puncta, and autophagy‐related protein ATG 9 transcription. These were all significantly reversed upon si RNA ‐mediated gene silencing of MT 1‐ MMP . ARP 101 can thus concomitantly inhibit MT 1‐ MMP extracellular catalytic function and exploit its intracellular transducing signal function to trigger autophagy‐mediated cell death in U87 glioblastoma cancer cells." @default.
• W2894930796 created "2018-10-12" @default.
• W2894930796 creator A5005866103 @default.
• W2894930796 creator A5061187310 @default.
• W2894930796 date "2018-10-30" @default.
• W2894930796 modified "2023-09-30" @default.
• W2894930796 title "Dual functions of ARP101 in targeting membrane type-1 matrix metalloproteinase: Impact on U87 glioblastoma cell invasion and autophagy signaling" @default.
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• W2894930796 doi "https://doi.org/10.1111/cbdd.13410" @default.
• W2894930796 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30291676" @default.
• W2894930796 hasPublicationYear "2018" @default.
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