Oncotarget

Research Perspectives:

miRNA signature of schwannomas: Possible role(s) of “tumor suppressor” miRNAs in benign tumors

Erdogan Pekcan Erkan, Xandra O. Breakefield and Okay Saydam _

PDF  |  HTML  |  How to cite  |  Order a Reprint

Oncotarget. 2011; 2:265-270. https://doi.org/10.18632/oncotarget.251

Metrics: PDF 2024 views  |   HTML 2402 views  |   ?  


Abstract

Erdogan Pekcan Erkan1, Xandra O. Breakefield2, and Okay Saydam1

1Molecular Oncology Research Unit, Division of Oncology, Department of Pediatrics, Medical University of Vienna, Vienna 1090 Austria

2Departments of Neurology and Radiology, Massachusetts General Hospital, and Neuroscience Program, Harvard Medical School, Boston, Massachusetts, 02129 USA

Keywords: miR-7, Tumor suppressor miRNAs, Benign tumors, Schwannomas, Neurofibromatosis 2 (NF2), Ack1

Received: March 30, 2011; Accepted: March 30, 2011; Published: March 30, 2011;

Correspondence:

Okay Saydam, e-mail:

Abstract

miRNAs have been recently implicated as drivers in several carcinogenic processes, where they can act either as oncogenes or as tumor suppressors. Schwannomas arise from Schwann cells, the myelinating cells of the peripheral nervous system. These benign tumors typically result from loss of the neurofibromatosis type 2 (NF2) tumor suppressor gene. We have recently carried out high-throughput miRNA expression profiling of human vestibular schwannomas using an array representing 407 known miRNAs in order to explore the role of miRNAs in the tumorigenesis of schwannomas. We found that miR-7 functions as a “tumor suppressor” by targeting proteins in three major oncogenic pathways - EGFR, Pak1, and Ack1. Interestingly, in this study, we also observed that several previously described potential tumor suppressor miRNAs that are down-regulated in malignant tumors were up-regulated in schwannomas. Here we discuss the possibility that “tumor suppressor” miRNAs may play a role in the transition stage(s) of cancer from benign to malignant forms.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 251