hsa-miR-9 controls the mobility behavior of glioblastoma cells via regulation of MAPK14 signaling elements
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Rotem Ben-Hamo1, Alona Zilberberg1, Helit Cohen1 and Sol Efroni1
1 The Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat-Gan, Israel
Sol Efroni, email:
Keywords: MAPKAP signaling, cytoskeleton, pathways, glioblastoma, metastasis, hsa-miR9
Received: July 23, 2015 Accepted: December 05, 2015 Published: December 21, 2015
Background: Glioblastoma Multiforme (GBM) is the most common and lethal primary tumor of the brain. GBM is associated with one of the worst 5-year survival rates among all human cancers, despite much effort in different modes of treatment.
Results: Here, we demonstrate specific GBM cancer phenotypes that are governed by modifications to the MAPAKAP network. We then demonstrate a novel regulation mode by which a set of five key factors of the MAPKAP pathway are regulated by the same microRNA, hsa-miR-9.
We demonstrate that hsa-miR-9 overexpression leads to MAPKAP signaling inhibition, partially by interfering with the MAPK14/MAPKAP3 complex. Further, hsa-miR-9 overexpression initiates re-arrangement of actin filaments, which leads us to hypothesize a mechanism for the observed phenotypic shift.
Conclusion: The work presented here exposes novel microRNA features and situates hsa-miR-9 as a therapeutic target, which governs metastasis and thus determines prognosis in GBM through MAPKAP signaling.
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