Hypermethylated long noncoding RNA MEG3 promotes the progression of gastric cancer

Ding, Lei; Tian, Yuan; Bi, Miaomiao; Teng, Dengke; Hong, Sen

doi:10.18632/aging.102309

Cited by 21 publications

(16 citation statements)

References 38 publications

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“…Studies on MEG3 in diabetic patients indicated that potential DNA methylation in the promoter region resulted in the reduction of target gene expression, thereby affecting disease development 38 . This was also observed in GC, where MEG3 levels are significantly lower and its methylation significantly greater in tumor cells than in para-cancerous tissues, as demonstrated in multiple GC cell lines 39 . Furthermore, DNA methylation affects the expression of MEG3 and its target miR-29 in HCC 40 .…”

Section: Multi-functional Roles Of Lncrnas In Gastric Cancersupporting

confidence: 53%

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Long non-coding RNAs in gastric cancer: New emerging biological functions and therapeutic implications

Tan

Zhang

et al. 2020

Theranostics

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Gastric cancer (GC) is currently the fourth most common malignancy and the third leading cause of cancer-related deaths worldwide. Long non-coding RNAs (lncRNAs), transcriptional products with more than 200 nucleotides, are not as well-characterized as protein-coding RNAs. Accumulating evidence has recently revealed that maladjustments of diverse lncRNAs may play key roles in multiple genetic and epigenetic phenomena in GC, affecting all aspects of cellular homeostasis, such as proliferation, migration, and stemness. However, the full extent of their functionality remains to be clarified. Considering the lack of viable biomarkers and therapeutic targets, future research should be focused on unravelling the intricate relationships between lncRNAs and GC that can be translated from bench to clinic. Here, we summarized the state-of-the-art advances in lncRNAs and their biological functions in GC, and we further discuss their potential diagnostic and therapeutic roles. We aim to shed light on the interrelationships between lncRNAs and GC with respect to their potential therapeutic applications. With better understanding of these relationships, the biological functions of lncRNAs in GC development will be exploitable, and promising new strategies developed for the prevention and treatment of GC.

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Section: Multi-functional Roles Of Lncrnas In Gastric Cancersupporting

confidence: 53%

“…Furthermore, DNA methylation affects the expression of MEG3 and its target miR-29 in HCC 40 . Similarly in GC, DNA methylation affects the expression of the MEG3 target miR-181a-5p, a tumor suppressor, thus downregulating the downstream target ATG4B (autophagy-associated 4B) 39 .…”

Section: Multi-functional Roles Of Lncrnas In Gastric Cancermentioning

confidence: 99%

Long non-coding RNAs in gastric cancer: New emerging biological functions and therapeutic implications

Tan

Zhang

et al. 2020

Theranostics

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“…MEG3 promoted glioma cell autophagy and inhibited cell proliferation and migration through positively regulating Sirt7 by inhibition of the PI3K/AKT/ mTOR signaling pathway [22]. The expression of MEG3 is controlled by epigenetics, and its gene is abnormally CpG-methylated in various tumors [23,24]. Furthermore, Mondal et al demonstrated that MEG3 and EZH2 shared common target genes [25].…”

Section: Ivyspringmentioning

confidence: 99%

Downregulation of MEG3 promotes neuroblastoma development through FOXO1-mediated autophagy and mTOR-mediated epithelial-mesenchymal transition

Ye¹,

Lü²,

Tang³

et al. 2020

Int. J. Biol. Sci.

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Our previous studies demonstrated that MEG3 was significantly downregulated in neuroblastoma (NB) and its expression was negatively associated with the INSS stage. Overexpression of MEG3 promoted apoptosis and inhibited proliferation in NB cells. In this study, we discovered more potential functions and molecular mechanisms of MEG3 in NB. According to the database, MEG3 positively correlated with the NB survival rate and was negatively associated with malignant clinical features. Moreover, we determined that MEG3 was mainly located in the nucleus by nuclear-cytoplasmic separation and RNA fish assays. Upregulation of MEG3 in stably transfected cell lines was accomplished, and CCK8, colony formation, and EDU assays were performed, which indicated that MEG3 significantly suppressed cell proliferation. Both wound healing and transwell experiments demonstrated that MEG3 decreased cell migration and invasion. CHIRP enrichments showed the anticancer effects of MEG3 were probably linked to autophagy and the mTOR signaling pathway. LC3 fluorescence dots and western blots showed that MEG3 attenuated autophagy by inhibiting FOXO1, but not the mTOR signaling pathway. Furthermore, MEG3 inhibited metastasis through epithelial-mesenchymal transition via the mTOR signaling pathway. Consistent with the above results, downregulation of MEG3 facilitated NB malignant phenotypes. Mechanistically, MEG3 and EZH2 regulated each other via a negative feedback loop and promoted NB progression together. In conclusion, our findings suggested that MEG3 was a tumor suppressor in NB and could be a potential target for NB treatment in the future.

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“…It has been reported that the expression of MEG3 was lower in GC tissues compared to adjacent normal tissues [ 10 ]. This downregulation is mediated by hypermethylation of the MEG3 promoter region which, in turn, provokes GC progression [ 13 , 14 ]. MEG3 not only regulates the p53 expression but also affects EMT, invasion, and migration of GC via sponging miRNAs including miR-181 and miR-21 by acting as a competing endogenous RNA (ceRNA) [ 15 – 17 ].…”

Section: Introductionmentioning

confidence: 99%

Expression of HOTAIR and MEG3 are negatively associated with H. pylori positive status in gastric cancer patients

et al. 2022

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Background: Chronic infection with Helicobacter pylori is one of the main causes of gastric cancer (GC). Besides, lncRNAs play crucial roles in cancer pathobiology including GC. Here we aimed to investigate the expression of MEG3 and HOTAIR in gastric cancer tissues and evaluate their association with the H. pylori status. Materials and Methods: One hundred samples were obtained. Total RNA was extracted, cDNA was synthesized and expression of MEG3 and HOTAIR was assessed using qRT-PCR. Association of their expression with H. pylori status and other clinicopathological characteristics were investigated. Furthermore, sensitivity and specificity of the MEG3 and HOTAIR expression levels for discrimination of the tumor and non-tumor samples were evaluated by Receiver operating characteristic (ROC) curve analysis. Results: We observed upregulation of HOTAIR but downregulation of MEG3 in tumor compared to the non-tumor tissues. We also found a significant negative association between their expression levels and H. pylori positive status. However, only the expression level of HOTAIR was significantly associated with the size and stage of the tumor ( P < 0.05). The ROC curve analysis revealed that the expression levels of MEG3 and HOTAIR might discriminate GC tumor and non-tumor tissues. Conclusions: In conclusion, this study revealed a negative association between H. pylori infection and expression of MEG3 and HOTAIR. The results suggested that the expression level of these lncRNAs might be considered as potential biomarkers for GC.

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Hypermethylated long noncoding RNA MEG3 promotes the progression of gastric cancer

Cited by 21 publications

References 38 publications

Long non-coding RNAs in gastric cancer: New emerging biological functions and therapeutic implications

Long non-coding RNAs in gastric cancer: New emerging biological functions and therapeutic implications

Downregulation of MEG3 promotes neuroblastoma development through FOXO1-mediated autophagy and mTOR-mediated epithelial-mesenchymal transition

Expression of HOTAIR and MEG3 are negatively associated with H. pylori positive status in gastric cancer patients

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