Oncotarget

Research Papers:

hsa-miR-9 controls the mobility behavior of glioblastoma cells via regulation of MAPK14 signaling elements

Rotem Ben-Hamo, Alona Zilberberg, Helit Cohen and Sol Efroni _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2016; 7:23170-23181. https://doi.org/10.18632/oncotarget.6687

Metrics: PDF 2291 views  |   HTML 2706 views  |   ?  


Abstract

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

Correspondence to:

Sol Efroni, email:

Keywords: MAPKAP signaling, cytoskeleton, pathways, glioblastoma, metastasis, hsa-miR9

Received: July 23, 2015 Accepted: December 05, 2015 Published: December 21, 2015

Abstract

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.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 6687