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©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Dec 28, 2007; 13(48): 6478-6491
Published online Dec 28, 2007. doi: 10.3748/wjg.v13.i48.6478
Published online Dec 28, 2007. doi: 10.3748/wjg.v13.i48.6478
JAK-STAT pathway in carcinogenesis: Is it relevant to cholangiocarcinoma progression
Olga V Smirnova, Tatiana Yu Ostroukhova, Laboratory of Endocrinology, Biological Faculty, M.V. Lomonosov Moscow State University, Moscow, Russia
Roman L Bogorad, Inserm, U845, Paris France; Université Paris Descartes, Faculté de Médecine René Descartes, Centre de Recherche Croissance et Signalisation, Equipe PRL, GH and tumours, Site Necker, Paris, F-75015, France
Correspondence to: Olga V Smirnova, PhD, DSc, Laboratory of Endocrinology, Biological Faculty, M.V. Lomonosov Moscow State University, Leninskie Gory, 1/12, 119992, Moscow, Russia. smirnova_ov@mail.ru
Telephone: +7-495-9393678 Fax: +7-495-9394309
Received: August 17, 2007
Revised: September 14, 2007
Accepted: September 26, 2007
Published online: December 28, 2007
Revised: September 14, 2007
Accepted: September 26, 2007
Published online: December 28, 2007
Abstract
The features of JAK-STAT signaling in liver cells are discussed in the current review. The role of this signaling cascade in carcinogenesis is accentuated. The possible involvement of this pathway and alteration of its elements are compared for normal cholangiocytes, cholangiocarcinoma predisposition and development. Prolactin and interleukin-6 are described in detail as the best studied examples. In addition, the non-classical nuclear translocation of cytokine receptors is discussed in terms of its possible implication to cholangiocarcinoma development.
Keywords: Cholangiocarcinoma, Janus tyrosine Kinases, Signal Transducers and Activators of Transcription, Prolactin, Interleukin-6, Cytokine receptors, Receptor tyrosine kinases