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Gene Therapy Leaves a Vicious Cycle
Reena Goswami1, Gayatri Subramanian2, Liliya Silayeva1, Isabelle Newkirk1, Deborah Doctor1, Karan Chawla2, Saurabh Chattopadhyay2, Dhyan Chandra3, Nageswararao Chilukuri1 and Venkaiah Betapudi1,4* 1Neuroscience Branch, Research Division, United States Army Medical Research Institute of Chemical Defense, Aberdeen, MD, United States 2Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, United States 3Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States 4Department of Physiology and Biophysics, Case Western Reserve University, Clev...
Source: Frontiers in Oncology - April 23, 2019 Category: Cancer & Oncology Source Type: research

Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway
In conclusion, our research results indicate that DAPT activates PI3K/AKT/Cdc42 signaling by non-canonical Notch pathway, and the activated Cdc42 promotes the filopodia formation and inhibits lamellipodia assembly, resulting in reduced migration of breast cancer cells. The results imply that non-canonical Notch signaling may play a very important role in the rapid response of cells to the extracellular signals. Author Contributions LG, JD, and LL designed the study and wrote and revised the manuscript. LL and LZ performed most of the experiments and data analysis. SZ, X-YZ, P-XM, Y-DM, Y-YW, YC, S-JT, and Y-JZ assisted i...
Source: Frontiers in Pharmacology - April 15, 2019 Category: Drugs & Pharmacology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Targeting of EGFR and HER2 with therapeutic antibodies and siRNA
Conclusion The epidermal growth factor receptor HER2 is a promising anti-tumor target for the therapy of glioblastoma. HER2 targeting may represent a promising strategy to induce cell physiological and radiobiological anti-tumor effects in glioblastoma.
Source: Strahlentherapie und Onkologie - January 29, 2015 Category: Cancer & Oncology Source Type: research

High epiregulin expression in human U87 glioma cells relies on IRE1alpha and promotes autocrine growth through EGF receptor
Conclusion: EREG may contribute to glioma progression under the control of IRE1alpha, as exemplified here by the autocrine proliferation loop mediated in U87 cells by the growth factor through ErbB1.
Source: BMC Cancer - December 13, 2013 Category: Cancer & Oncology Authors: Gregor AufArnaud JabouilleMaylis DeluginSylvaine GuéritRaphael PineauSophie NorthNatalia PlatonovaMarlène MaitreAlexandre FavereauxPeter VajkoczyMasaharu SenoAndreas BikfalviDmitri MinchenkoOleksandr MinchenkoMichel Moenner Source Type: research

High epiregulin expression in human U87 glioma cells relies on IRE1¿ and promotes autocrine growth through EGF receptor
Conclusion: EREG may contribute to glioma progression under the control of IRE1alpha, as exemplified here by the autocrine proliferation loop mediated in U87 cells by the growth factor through ErbB1.
Source: BMC Cancer - December 13, 2013 Category: Cancer & Oncology Authors: Gregor AufArnaud JabouilleMaylis DeluginSylvaine GuéritRaphael PineauSophie NorthNatalia PlatonovaMarlène MaitreAlexandre FavereauxPeter VajkoczyMasaharu SenoAndreas BikfalviDmitri MinchenkoOleksandr MinchenkoMichel Moenner Source Type: research