Journal
CANCER CELL
Volume 20, Issue 2, Pages 229-245Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2011.06.018
Keywords
-
Categories
Funding
- Cancer Research UK
- EU
- French Society of Dermatological Research (SRD)
- INSERM
- NHS
- Cancer Research UK [12065] Funding Source: researchfish
Ask authors/readers for more resources
Proinflammatory cytokines are frequently observed in the tumor microenvironment, and chronic inflammation is involved in cancer initiation and progression. We show that cytokine signaling through the receptor subunit GP130-IL6ST and the kinase JAK1 generates actomyosin contractility through Rho-kinase dependent signaling. This pathway generates contractile force in stromal fibroblasts to remodel the extracellular matrix to create tracks for collective migration of squamous carcinoma cells and provides the high levels of actomyosin contractility required for migration of individual melanoma cells in the rounded, amoeboid mode. Thus, cytokine signaling can generate actomyosin contractility in both stroma and tumor cells. Strikingly, actomyosin contractility itself positively modulates activity of the transcription factor STAT3 downstream of JAK1, demonstrating positive feedback within the signaling network.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available