TOPIC REVIEW MEG3: a novel long noncoding potentially tumour-suppressing RNA in meningiomas Vladimir Balik • Josef Srovnal • Igor Sulla • Ondrej Kalita • Tatiana Foltanova • Miroslav Vaverka • Lumir Hrabalek • Marian Hajduch Received: 19 September 2012 / Accepted: 29 December 2012 / Published online: 11 January 2013 Ó Springer Science+Business Media New York 2013 Abstract Meningiomas represent one of the most com- mon types of primary intracranial tumours. However, the specific molecular mechanisms underlying their patho- genesis remain uncertain. Loss of chromosomes 22q, 1p, and 14q have been implicated in most meningiomas. Inactivation of the NF2 gene at 22q12 has been identified as an early event in their pathogenesis, whereas abnormalities of chromosome 14 have been reported in higher-grade as well as recurrent tumours. It has long been supposed that chromosome 14q32 contains a tumour suppressor gene. However, the identity of the potential 14q32 tumour suppressor remained elusive until the Maternally Expressed Gene 3 (MEG3) was recently sug- gested as an ideal candidate. MEG3 is an imprinted gene located at 14q32 that encodes a non-coding RNA (ncRNA). In meningiomas, loss of MEG3 expression, its genomic DNA deletion and degree of promoter methylation have been found to be associated with aggressive tumour growth. These findings indicate that MEG3 may have a significant role as a novel long noncoding RNA tumour suppressor in meningiomas. Keywords Maternally Expressed Gene 3 Non-coding RNA Á Meningiomas General considerations Although the term meningioma was coined by Harvey Cushing in 1922 to describe a benign tumour of meninges [1], based on World Health Organization (WHO) classifi- cation, meningiomas are graded as either grade I, II or III [2, 3]. They are generally thought to rise from arachnoidal cap cells [4] and progress from low-grade to high-grade tumours due to numerous genetic abnormalities. Complete removal of benign meningiomas constitutes a cure for the patient. However, long-term follow-up has shown that the recurrence rate of histologically benign cranial base meningiomas, even after radiologically confirmed total resection, is 4–26 % [5, 6]. The 3-, 5- and 10-year recur- rence rates of patients with subtotally resected WHO grade I tumours, range from 23–50 %, 37–60 % and 55–100 %, respectively [7]. The 5-year recurrence rate of WHO grade II tumours may be as high as 41 %, even following a Simpson grade I resection, and this high recurrence rate is associated with an increased risk of death (around 14 and 31 % at 5 and 10 years, respectively) [8]. Patients with a WHO grade III meningioma currently have few treatment options, as surgery combined with high-dose adjuvant fractionated radiotherapy is associated with a recurrence risk of 80 % at 5 years and a substantial risk of disease-related death [7]. Furthermore, because of the complex structure of V. Balik (&) Á O. Kalita Á M. Vaverka Á L. Hrabalek Department of Neurosurgery, Faculty Hospital Olomouc, I.P. Pavlova 6, 775 20 Olomouc, Czech Republic e-mail: balik.vladimir@gmail.com J. Srovnal Á M. Hajduch Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University and Faculty Hospital Olomouc, Hne ˇvotı ´nska ´ 5, 775 15 Olomouc, Czech Republic I. Sulla Department of Anatomy, Histology and Physiology, University of Veterinary Medicine and Pharmacy in Kosice, Komenskeho 73, 041 81 Kosice, Slovak Republic T. Foltanova Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University in Bratislava, Kalinc ˇiakova ul. 8, 832 32 Bratislava, Slovak Republic 123 J Neurooncol (2013) 112:1–8 DOI 10.1007/s11060-012-1038-6