Sequential Ras/MAPK and PI3K/AKT/mTOR pathways recruitment drives basal extrusion in the prostate-like gland of Drosophila.
Animals
Drosophila
Drosophila Proteins
/ metabolism
Exocrine Glands
/ metabolism
Male
Mitogen-Activated Protein Kinases
/ metabolism
Phosphatidylinositol 3-Kinases
/ metabolism
Prostatic Neoplasms
/ metabolism
Proto-Oncogene Proteins c-akt
/ metabolism
Signal Transduction
/ physiology
TOR Serine-Threonine Kinases
/ metabolism
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
08 05 2020
08 05 2020
Historique:
received:
29
03
2016
accepted:
16
04
2020
entrez:
10
5
2020
pubmed:
10
5
2020
medline:
18
8
2020
Statut:
epublish
Résumé
One of the most important but less understood step of epithelial tumourigenesis occurs when cells acquire the ability to leave their epithelial compartment. This phenomenon, described as basal epithelial cell extrusion (basal extrusion), represents the first step of tumour invasion. However, due to lack of adequate in vivo model, implication of emblematic signalling pathways such as Ras/Mitogen-Activated Protein Kinase (MAPK) and phosphoinositide 3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signalling pathways, is scarcely described in this phenomenon. We have developed a unique model of basal extrusion in the Drosophila accessory gland. There, we demonstrate that both Ras/MAPK and PI3K/AKT/mTOR pathways are necessary for basal extrusion. Furthermore, as in prostate cancer, we show that these pathways are co-activated. This occurs through set up of Epidermal Growth Factor Receptor (EGFR) and Insulin Receptor (InR) dependent autocrine loops, a phenomenon that, considering human data, could be relevant for prostate cancer.
Identifiants
pubmed: 32385236
doi: 10.1038/s41467-020-16123-w
pii: 10.1038/s41467-020-16123-w
pmc: PMC7210301
doi:
Substances chimiques
Drosophila Proteins
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
TOR Serine-Threonine Kinases
EC 2.7.11.1
Mitogen-Activated Protein Kinases
EC 2.7.11.24
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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