Cancer exosomes induce tumor neo-neurogenesis potentiating tumor growth
Posted on: 30 January 2018 , updated on: 23 February 2018
Preprint posted on 1 December 2018
Extracellular vesicles (EVs) loaded with EphrinB1 drive tumor innervation and subsequent tumor growth
Selected by Jacky G. Goetz
Categories: cancer biology, cell biology
Summary
Extracellular vesicles (EVs) loaded with EphrinB1 drive tumor innervation and subsequent tumor growth
This preprint from the group of Paola Vermeer identifies a new role – innervation that fosters growth – for EVs in tumor progression. This interesting and newly identified role adds to a wide list of pro-tumorigenic functions carried out by EVs. Although anti- and pro-tumorigenic functions have been attributed to tumor-released EVs, these new observations identify EVs as a new means used by tumors to exchange information with nerve fibers.
Bigger picture
This study focuses on a concept – neo-neurogenesis during tumor growth – that has been, in comparison to angiogenesis and lymphangiogenesis, only poorly studied so far. While tumors are known to release neurotrophic factors during growth, the authors reasoned that tumors might have additional mechanisms to secrete functional components driving neo-neurogenesis. Although the reason for this is not fully clear, the authors focused here on EphrinB1, which is an axonal guidance molecule. It is well known that innervation of tumors makes them more aggressive. In addition, tumor innervation could play influential roles in the regulation of immune responses and tumor surveillance. Understanding the mechanisms driving neo-neurogenesis is thus of clinical relevance.
Open questions
Does such a mechanism apply to several tumor types ?
Are there other neurotrophic/guidance molecule factors that could be selectively loaded on EVs ?
Why would tumor neo-neurogenesis require EVs, in addition to classical neurotrophic factors ?
How could we inhibit uptake of EVs in tumor-associated ?
Related references
- Magnon et al., Autonomic nerve development contributes to prostate cancer progression. Science 341, 1236361 (2013).
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