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Breaking the oncostatin M feed‐forward loop to suppress metastasis and therapy failure
Author(s) -
Smigiel Jacob,
Parvani Jenny G,
Tamagno Ilaria,
Polak Kelsey,
Jackson Mark W
Publication year - 2018
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.5063
Subject(s) - oncostatin m , metastasis , cancer research , interleukin 6 , tumor microenvironment , cancer , carcinogenesis , medicine , biology , bioinformatics , cytokine , immunology , tumor cells
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.