non-canonical smads phosphorylation induced by the glutamate release inhibitor, riluzole, through gsk3 activation in melanoma谷氨酸释放引起的非规范smads磷酸化抑制剂,gsk3利鲁唑,通过激活黑素瘤.pdfVIP

Non-Canonical Smads Phosphorylation Induced by the Glutamate Release Inhibitor, Riluzole, through GSK3 Activation in Melanoma 1. 1. 2 1 2 Walid Abushahba , Oyenike O. Olabisi , Byeong-Seon Jeong , Rajeev K. Boregowda , Yu Wen , 3 2 4 1 Fang Liu , James S. Goydos , Ahmed Lasfar , Karine A. Cohen-Solal * 1 Department of Medicine, Division of Medical Oncology, University of Medicine and Dentistry of New Jersey - Robert Wood Johnson Medical School, The Cancer Institute of New Jersey, New Brunswick, New Jersey, United States of America, 2 Department of Surgery, Division of Surgical Oncology, University of Medicine and Dentistry of New Jersey - Robert Wood Johnson Medical School, The Cancer Institute of New Jersey, New Brunswick, New Jersey, United States of America, 3 Center for Advanced Biotechnology and Medicine, Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey, United States of America, 4 Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey, United States of America Abstract Riluzole, an inhibitor of glutamate release, has shown the ability to inhibit melanoma cell xenograft growth. A phase 0 clinical trial of riluzole as a single agent in patients with melanoma resulted in involution of tumors associated with inhibition of both the mitogen-activated protein kinase (MAPK) and phophoinositide-3-kinase/AKT (PI3K/AKT) pathways in 34% of patients.