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Colorectal cancer cell–derived exosomes containing miR-10b regulate fibroblast cells via the PI3K/Akt pathway / Guangyao Dai in Bulletin du cancer, vol. 105, 4 (Avril-juin 2018)
[article]
in Bulletin du cancer > vol. 105, 4 (Avril-juin 2018) . - p. 336-349
Titre : Colorectal cancer cell–derived exosomes containing miR-10b regulate fibroblast cells via the PI3K/Akt pathway Type de document : article de périodique Auteurs : Guangyao Dai ; Xiaoguang Yao ; Yubin Zhang Année de publication : 2018 Article en page(s) : p. 336-349 Note générale : https://doi.org/10.1016/j.bulcan.2017.12.009 Langues : Français (fre) Descripteurs (mots clés) : [Thésaurus Mesh]:T:Tumeurs colorectales:Tumeurs colorectales / physiopathologie
[Thésaurus Mesh]Carcinogenèse
[Thésaurus Mesh]Exosomes
[Thésaurus Mesh]Fibroblastes associés au cancer
[Thésaurus Mesh]MicroARNMots-clés : Fibroblastes associés au cancer Tumeurs colorectales / physiopathologie Carcinogenèse Exosomes MicroARN MiR-10b PIK3CA PI3K/Akt/mTOR pathway Résumé : Background
Cancer-associated fibroblasts (CAFs) contribute to the proliferation of colorectal cancer(CRC) cells. However, the mechanism by which CAFs develop in the tumor microenvironment remains unknown. Exosomes may be involved in activating CAFs.
Methods
Using a miRNA expression profiling array, we determined the miRNA expression profile of secretory exosomes in CRC cells and then identified potential miRNAs with significant differential expression compared to normal cells via enrichment analysis. Predicted targets of candidate miRNAs were then assessed via bioinformatics analysis. Realtime qPCR, western blot, and cell cycle analyses were performed to evaluate the role of candidate exosomal miRNAs. Luciferase reporter assays were applied to confirm whether candidate exosomal miRNAs control target pathway expression. A CRC xenograft mouse model was constructed to evaluate tumor growth in vivo.
Results
Exosomes from CRC cells contained significantly higher levels of miR-10b than did exosomes from normal colorectal epithelial cells. Moreover, exosomes containing miR-10b were transferred to fibroblasts. Bioinformatics analysis identified PIK3CA, as a potential target of miR-10b. Luciferase reporter assays confirmed that miR-10b directly inhibited PIK3CA expression. Co-culturing fibroblasts with exosomes containing miR-10b significantly suppressed PIK3CA expression and decreased PI3K/Akt/mTOR pathway activity. Finally, exosomes containing miR-10b reduced fibroblast proliferation but promoted expression of TGF-? and SM ?-actin, suggesting that exosomal miR-10b may activate fibroblasts to become CAFs that express myofibroblast markers. These activated fibroblasts were able to promote CRC growth in vitro and in vivo.
Conclusion
CRC-derived exosomes actively promote disease progression by modulating surrounding stromal cells, which subsequently acquire features of CAFs.Permalink : https://bibliotheque.helb-prigogine.be/opac_css/index.php?lvl=notice_display&id= [article]Exemplaires
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