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Breaking the oncostatin M feed-forward loop to suppress metastasis and therapy failure
Jacob Smigiel1, Jenny G Parvani1, Ilaria Tamagno1
1Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA.
Abstract:
Deciphering the complex milieu that makes up the tumor microenvironment (TME) and the signaling engaged by TME cytokines continues to provide novel targets for therapeutic intervention. The IL-6 family member oncostatin M (OSM) has recently emerged as a potent driver of tumorigenesis, metastasis, and therapy failure, molecular programs most frequently attributed to IL-6 itself. In a recent issue of The Journal of Pathology, Kucia-Tran et al describe how elevated oncostatin M receptor (OSMR) expression results in a feed-forward loop involving the de novo production of both OSM and OSMR to facilitate aggressive properties in squamous cell carcinoma (SCC). Here, we discuss how new findings implicating OSM in conferring aggressive cancer cell properties can be leveraged to suppress metastatic outgrowth and therapy failure in SCC as well as other cancers. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Insights
Oncostatin M (OSM) drives aggressive cancer properties by creating a feed-forward loop with its receptor (OSMR). This discovery offers new therapeutic targets to combat tumor growth and treatment resistance in squamous cell carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The tumor microenvironment (TME) and its cytokines are crucial for cancer progression.
- Oncostatin M (OSM), an IL-6 family cytokine, is increasingly recognized for its role in tumorigenesis and therapy failure.
- Understanding OSM signaling is vital for developing new cancer treatments.
Purpose of the Study:
- To investigate the role of oncostatin M receptor (OSMR) in squamous cell carcinoma (SCC).
- To elucidate the feed-forward loop mechanism involving OSM and OSMR in aggressive cancer phenotypes.
- To identify potential therapeutic strategies targeting the OSM/OSMR axis.
Main Methods:
- Analysis of OSMR expression in SCC.
- Investigation of the de novo production of OSM and OSMR.
- Characterization of the functional consequences of the OSM/OSMR loop on cancer cell aggressiveness.
Main Results:
- Elevated OSMR expression was observed in SCC.
- A feed-forward loop of OSM and OSMR production was identified, promoting aggressive cancer properties.
- This loop contributes to metastasis and therapeutic resistance in SCC.
Conclusions:
- The OSM/OSMR axis plays a significant role in driving aggressive SCC.
- Targeting this feed-forward loop presents a promising therapeutic avenue to overcome metastatic outgrowth and treatment failure.
- Further research into OSM signaling can yield novel strategies for various cancer types.
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