Abstract
LncRNAs are emerging as integral functional and regulatory components of normal biological activities and are now considered as critically involved in the development of different diseases including cancer. In this review, we summarized recent findings on maternally expressed gene 3 (MEG3), a noncoding lncRNA, locates in the imprinted DLK1–MEG3 locus on human chromosome 14q32.3 region. MEG3 is expressed in normal tissues but is either lost or decreased in many human tumors and tumor derived cell lines. Studies have demonstrated that MEG3 is associated with cancer initiation, progression, metastasis and chemo-resistance. MEG3 may affect the activities of TP53, MDM2, GDF15, RB1 and some other key cell cycle regulators. In addition, the level of MEG3 showed good correlation with cancer clinicopathological grade. In summary, MEGs is an RNA-based tumor suppressor and is involved in the etiology, progression, and chemosensitivity of cancers. The alteration of MEG3 levels in various cancers suggested the possibility of using MEG3 level for cancer diagnosis and prognosis.
Highlights
Cancer is one of the main causes of death worldwide
A number of independent studies have demonstrated the involvement of noncoding RNAs, such as small nucleolar RNAs, microRNAs, as well as long noncoding RNAs in cancer development [1,2,3]
Recent studies suggest some long noncoding RNAs (lncRNAs) such as GAS5, p21, H19, HOTAIR and PTENP1 may play a role in tumor suppression by affecting cell proliferation, invasion and metastasis [11,12,13,14,15,16]
Summary
Cancer is one of the main causes of death worldwide. A number of independent studies have demonstrated the involvement of noncoding RNAs, such as small nucleolar RNAs (snoRNAs), microRNAs (miRNAs), as well as long noncoding RNAs (lncRNAs) in cancer development [1,2,3]. Astuti et al showed that the MEG3-DMR is completely methylated in neuroblastoma cell lines and hypermethylated MEG3 promoter is associated with down regulation of MEG3 and upregulation of DLK1 expression [31]. Decreased expression of MEG3 contributes to retinoblastoma progression and affects retinoblastoma cell growth by regulating the activity of Wnt/β-catenin pathway.
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