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Agonist-Mediated Activation Of Sting Induces Apoptosis In Malignant B Cells, Chih-Hang Anthony Tang, Joseph A. Zundell, Sujeewa Ranatunga, Cindy Lin, Yulia Nefedova, Juan R. Del Valle, Chih-Chi Andrew Hu
Agonist-Mediated Activation Of Sting Induces Apoptosis In Malignant B Cells, Chih-Hang Anthony Tang, Joseph A. Zundell, Sujeewa Ranatunga, Cindy Lin, Yulia Nefedova, Juan R. Del Valle, Chih-Chi Andrew Hu
Chemistry Faculty Publications
Endoplasmic reticulum (ER) stress responses through the IRE-1/XBP-1 pathway are required for the function of STING (TMEM173), an ER-resident transmembrane protein critical for cytoplasmic DNA sensing, IFN production, and cancer control. Here we show that the IRE-1/XBP-1 pathway functions downstream of STING and that STING agonists selectively trigger mitochondria-mediated apoptosis in normal and malignant B cells. Upon stimulation, STING was degraded less efficiently in B cells, implying that prolonged activation of STING can lead to apoptosis. Transient activation of the IRE-1/XBP-1 pathway partially protected agonist-stimulated malignant B cells from undergoing apoptosis. In Eμ-TCL1 mice with chronic lymphocytic leukemia, injection of …
The Jak2 Small Molecule Inhibitor, G6, Reduces The Tumorigenic Potential Of T98g Glioblastoma Cells In Vitro And In Vivo, Rebekah Baskin, Sung O. Park, György M. Keserű, Kirpal S. Bisht, Heather L. Wamsley, Peter P. Sayeski
The Jak2 Small Molecule Inhibitor, G6, Reduces The Tumorigenic Potential Of T98g Glioblastoma Cells In Vitro And In Vivo, Rebekah Baskin, Sung O. Park, György M. Keserű, Kirpal S. Bisht, Heather L. Wamsley, Peter P. Sayeski
Chemistry Faculty Publications
Glioblastoma multiforme (GBM) is the most common and the most aggressive form of primary brain tumor. Jak2 is a non-receptor tyrosine kinase that is involved in proliferative signaling through its association with various cell surface receptors. Hyperactive Jak2 signaling has been implicated in numerous hematological disorders as well as in various solid tumors including GBM. Our lab has developed a Jak2 small molecule inhibitor known as G6. It exhibits potent efficacy in vitro and in several in vivo models of Jak2-mediated hematological disease. Here, we hypothesized that G6 would inhibit the pathogenic growth of GBM cells expressing hyperactive Jak2. To …