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Cdc42EP3/BORG2 and Septin Network Enables Mechano-transduction and the Emergence of Cancer-Associated Fibroblasts.

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Publication Date
2015-12-29
ICR Author
Calvo, Fernando
Ranftl, Romana
Farrugia, Aaron
Author
Calvo, F
Ranftl, R
Hooper, S
Farrugia, AJ
Moeendarbary, E
Bruckbauer, A
Batista, F
Charras, G
Sahai, E
Type
Journal Article
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Abstract
Cancer-associated fibroblasts (CAFs) are non-cancerous cells found in solid tumors that remodel the tumor matrix and promote cancer invasion and angiogenesis. Here, we demonstrate that Cdc42EP3/BORG2 is required for the matrix remodeling, invasion, angiogenesis, and tumor-growth-promoting abilities of CAFs. Cdc42EP3 functions by coordinating the actin and septin networks. Furthermore, depletion of SEPT2 has similar effects to those of loss of Cdc42EP3, indicating a role for the septin network in the tumor stroma. Cdc42EP3 is upregulated early in fibroblast activation and precedes the emergence of the highly contractile phenotype characteristic of CAFs. Depletion of Cdc42EP3 in normal fibroblasts prevents their activation by cancer cells. We propose that Cdc42EP3 sensitizes fibroblasts to further cues-in particular, those activating actomyosin contractility-and thereby enables the generation of the pathological activated fibroblast state.
URL
https://repository.icr.ac.uk/handle/internal/333
Collections
  • Cancer Biology
Version of record
10.1016/j.celrep.2015.11.052
Subject
Animals
Cell Line
Cell Line, Tumor
Fibroblasts
GTP-Binding Protein Regulators
Humans
Mice
Neoplasms
Septins
Up-Regulation
cdc42 GTP-Binding Protein
Research team
Tumour Microenvironment
Language
eng
Date accepted
2015-11-16
License start date
2015-12-29
Citation
Cell Rep, 2015, 13 (12), pp. 2699 - 2714

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