Navigation überspringen
Universitätsbibliothek Heidelberg
Standort: ---
Exemplare: ---
heiBIB
 Online-Ressource
Verfasst von:Göhring, Axel Robert [VerfasserIn]   i
 Cheng, Xinlai [VerfasserIn]   i
 Theobald, Jannick [VerfasserIn]   i
 Wölfl, Stefan [VerfasserIn]   i
Titel:Human microRNA-299-3p decreases invasive behavior of cancer cells by downregulation of Oct4 expression and causes apoptosis
Verf.angabe:Axel R. Göhring, Stefanie Reuter, Joachim H. Clement, Xinlai Cheng, Jannick Theobald, Stefan Wölfl, Ralf Mrowka
Fussnoten:Gesehen am 21.06.2017
Titel Quelle:Enthalten in: Public Library of Science: PLoS one
Jahr Quelle:2017
Band/Heft Quelle:12(2017,4) Artikel-Nummer e0174912, 15 Seiten
ISSN Quelle:1932-6203
Abstract:Purpose Oct4 was reported to be one of the most important pluripotency transcription factors in the biology of stem cells including cancer stem cells, and progressed malignant cells. Here we report the investigation of gene expression control of Oct4 by selected human microRNAs and the physiological effect of Oct4 silencing in invasive cancer cells. Methods and results High throughput luciferase activity assay revealed the microRNA-299-3p to be the most effective in reducing gene expression of Oct4, which was confirmed by Western blot analysis and Oct4 promoter activity in a target luciferase assay. Furthermore, it could be demonstrated that downregulation of Oct4 by microRNAs-299-3p in breast cancer and fibrosarcoma cells lead to a decreased invasiveness in a microfluidic chip assay. Additionally, microRNA-299-3p causes apoptosis in cancer cells. Comparison with Oct4 specific siRNA transfection confirmed that this effect is primary due to the blockade of Oct4 expression.Conclusion The results suggest that microRNA-299-3p is an interesting target for potential clinical use. It may be able to decrease invasive behaviour of carcinoma cells; or even kill these cells by causing apoptosis.
DOI:doi:10.1371/journal.pone.0174912
URL:Kostenfrei: Verlag: http://dx.doi.org/10.1371/journal.pone.0174912
 Kostenfrei: Verlag: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0174912
 DOI: https://doi.org/10.1371/journal.pone.0174912
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1560042508
Verknüpfungen:→ Zeitschrift
 
 
Lokale URL UB: Zum Volltext

Permanenter Link auf diesen Titel (bookmarkfähig):  https://katalog.ub.uni-heidelberg.de/titel/68130005   QR-Code
zum Seitenanfang