Abstract
Background: The gp130 cytokine, oncostatin M (OSM), serves several physiological and pathological functions. At the molecular level, OSM can directly or indirectly participate in tumorigenesis and insulin resistance development. Although OSM was initially found to be anti-proliferative in tumors, numerous tumorigenic roles for OSM have been reported in a variety of cancers. In metabolic diseases, OSM signaling may be required for homeostasis in both the liver and the adipose tissue, since abrogation of OSM signaling causes obesity, hepatic steatosis, and insulin resistance. This review aims to: 1) examine the current literature regarding the role of OSM in the development of cancers and insulin resistance; and 2) propose a possible link between cancerassociated OSM and the development of the insulin resistance observed with cancer cachexia.
Conclusion: In light of the potential links between cancer-associated OSM and cachexia-related insulin resistance, additional research is needed, especially given the possible link between these disease states. When considering OSM as a pharmaceutical target, its tumorigenic effects and role in tissue homeostasis must be carefully considered.
Keywords: Oncostatin M, gp130 cytokines, obesity, insulin resistance, cancer, tumorigenesis.
Current Pharmaceutical Design
Title:Oncostatin M: Potential Implications for Malignancy and Metabolism
Volume: 23 Issue: 25
Author(s): Jacqueline M. Stephens and Carrie M. Elks*
Affiliation:
- Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA, 70808,United States
Keywords: Oncostatin M, gp130 cytokines, obesity, insulin resistance, cancer, tumorigenesis.
Abstract: Background: The gp130 cytokine, oncostatin M (OSM), serves several physiological and pathological functions. At the molecular level, OSM can directly or indirectly participate in tumorigenesis and insulin resistance development. Although OSM was initially found to be anti-proliferative in tumors, numerous tumorigenic roles for OSM have been reported in a variety of cancers. In metabolic diseases, OSM signaling may be required for homeostasis in both the liver and the adipose tissue, since abrogation of OSM signaling causes obesity, hepatic steatosis, and insulin resistance. This review aims to: 1) examine the current literature regarding the role of OSM in the development of cancers and insulin resistance; and 2) propose a possible link between cancerassociated OSM and the development of the insulin resistance observed with cancer cachexia.
Conclusion: In light of the potential links between cancer-associated OSM and cachexia-related insulin resistance, additional research is needed, especially given the possible link between these disease states. When considering OSM as a pharmaceutical target, its tumorigenic effects and role in tissue homeostasis must be carefully considered.
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Cite this article as:
Stephens M. Jacqueline and Elks M. Carrie*, Oncostatin M: Potential Implications for Malignancy and Metabolism, Current Pharmaceutical Design 2017; 23 (25) . https://dx.doi.org/10.2174/1381612823666170704122559
DOI https://dx.doi.org/10.2174/1381612823666170704122559 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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