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Oncostatin M: Potential Implications for Malignancy and Metabolism
Jacqueline M Stephens1, Carrie M Elks1
1Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA, 70808. United States.
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.
Insights
Oncostatin M (OSM) plays a dual role in cancer and metabolic diseases. This review explores OSM's involvement in tumorigenesis and insulin resistance, suggesting a link between cancer-associated OSM and cachexia-related insulin resistance.
Area of Science:
- Biochemistry
- Molecular Biology
- Endocrinology
Background:
- Oncostatin M (OSM), a gp130 cytokine, has diverse physiological and pathological roles.
- OSM is implicated in both cancer development and the pathogenesis of insulin resistance.
- While initially considered anti-proliferative in tumors, OSM now shows significant tumorigenic roles in various cancers.
Purpose of the Study:
- To review the literature on OSM's role in cancer development.
- To examine OSM's contribution to insulin resistance.
- To propose a connection between cancer-associated OSM and insulin resistance in cancer cachexia.
Main Methods:
- Literature review of existing studies on OSM.
- Analysis of OSM signaling pathways in cancer.
- Examination of OSM's impact on metabolic homeostasis.
Main Results:
- OSM signaling is crucial for liver and adipose tissue homeostasis.
- Disruption of OSM signaling leads to obesity, hepatic steatosis, and insulin resistance.
- Evidence suggests OSM contributes to tumorigenesis across multiple cancer types.
Conclusions:
- Further research is needed to elucidate the link between cancer-associated OSM and cachexia-related insulin resistance.
- OSM's dual role in tumorigenesis and tissue homeostasis requires careful consideration for therapeutic targeting.
- Understanding OSM's complex functions is critical for managing cancer and metabolic disorders.
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