title: ERK plays the baddie (again).
abstract: It has been known for many years that elevated signaling by the ERK1/2 pathway is frequently associated with the growth and survival of many tumor cell types under a variety of normal and stressful conditions, including the response of cells to other cancer interventional therapeutic strategies e.g., references 1–4. There is, however, a modest significant literature showing that enhanced ERK1/2 signaling can also cause tumor cell death e.g., references 5–8. The role of ERK1/2 signaling is clearly complex, for example as shown by the Koumenis group where inhibition of radiation-induced ERK1/2 signaling caused radiosensitization, whereas inhibition of curcumin-hyper-stimulated ERK1/2 signaling reduced radiosensitivity. 7 Presumably this Janus-faced behavior of the ERK1/2 pathway in terms of cell survival regulation will depend upon the tumor cell type, the intensity of ERK1/2 stimulation, and the molecular intervention/drug being used.
authors.affiliation: Department of Neurosurgery; Massey Cancer Center; Virginia Commonwealth University; Richmond, VA USA.
authors.forename: Paul
authors.initials: P
authors.lastname: Dent
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism*; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002166:Camptothecin / Q000494:pharmacology*; D003110:Colonic Neoplasms / Q000378:metabolism*; D054638:Dual Specificity Phosphatase 1 / Q000378:metabolism*; D006801:Humans; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D054638:Dual Specificity Phosphatase 1; D002166:Camptothecin
keywords: ERK; MKP1; camptothecin; human colon cancer
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