Long noncoding RNA MEG3 play an important role in osteosarcoma development through sponging microRNAs

Jiang, Ming; Xu, Nan; Zhou, Lei; An, Qing

doi:10.1002/jcb.27791

Cited by 20 publications

(13 citation statements)

References 40 publications

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“…FYN and β-catenin are reported to be responsible for the development and progression of OS [16,17]. Interesting, they were predicted to directly or indirectly interact with FES using the STRING database (https ://strin g-db.org/).…”

Section: Western Blot Analysismentioning

confidence: 99%

Overexpression of FES might inhibit cell proliferation, migration, and invasion of osteosarcoma cells

Zhao

Wang

et al. 2020

Cancer Cell Int

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Background: This study aimed to screen osteosarcoma (OS) prognosis relevant genes for methylation dysregulation, and the functional mechanisms of FES overexpression in OS cells were investigated. Methods: The OS prognosis relevant genes with differentially methylated positions (DMPs) identified from the GSE36001 and GSE36002 datasets, and the UCSC database, were used as a training set to construct a risk model, while the GSE21257 dataset was used as validation set. The expression levels of several key genes in OS cells after 5-Aza-2′-deoxycytidine treatment were detected by qPCR. The effects of FES overexpression on cell proliferation, cell cycle, migration, and invasion of MNNG/HOS were analyzed by CCK8, flow cytometry, and Transwell assays. Results: A total of 31 candidate genes, corresponding to 36 DMPs, were identified as OS prognosis relevant genes; from these, the top 10 genes were used to construct a risk model. Following validation of the risk model, FES, LYL1, MAP4K1, RIPK3, SLC15A3, and STAT3 showed expression changes between the OS and control samples. qPCR results showed that the expression of FES was significantly downregulated in three OS cell lines and increased after 5-Aza-DC treatment. The proliferation, cell cycle progression, migration, and invasion of MNNG/HOS cells were significantly inhibited after transfection with FES overexpression plasmid, and the protein expression of FYN and β catenin were decreased in MNNG/HOS cells by FES overexpression. Conclusions: The decrease in FES by hypermethylation was associated with OS prognosis, and might contribute to the proliferation, migration, and invasion of OS cells. FES, and its upstream FYN and β catenin, might coordinately exert a tumor suppressor effect in OS cells.

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Section: Western Blot Analysismentioning

confidence: 99%

Overexpression of FES might inhibit cell proliferation, migration, and invasion of osteosarcoma cells

Zhao

Wang

et al. 2020

Cancer Cell Int

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“…It has been shown that lncRNAs are aberrantly expressed in OS tissues and dysregulated expression is associated with clinical outcomes and disease status (36,37). Studies have shown that lncRNAs which exhibit dysregulated expression may serve as prognostic biomarkers and therapeutic targets for patients with OS (12,27).…”

Section: Roles Of Lncrna Meg3 In Bone Diseasesmentioning

confidence: 99%

“…An increasing number of studies have shown that MEG3 serves an important role in the development of osteogenic differentiation and thus regulates bone formation, metabolism, and regeneration (10,11). Additionally, dysregulation of MEG3 is associated with various bone diseases including bone tumors, joint degeneration, osteoporosis and rheumatoid arthritis (RA) (12)(13)(14)(15). To the best of our knowledge, there are no literature reviews summarizing the specific roles of MEG3 in the development of osteogenic differentiation and bone diseases.…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA MEG3 is involved in osteogenic differentiation and bone diseases (Review)

Sun

Peng

et al. 2020

Biomed Rep

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Osteogenic differentiation originating from mesenchymal stem cells (MSCs) requires tight coordination of transcriptional factors, signaling pathways and biomechanical cues. Dysregulation of such reciprocal networks may influence the proliferation and apoptosis of MSCs and osteoblasts, thereby impairing bone metabolism and homeostasis. An increasing number of studies have shown that long non-coding (lnc)RNAs are involved in osteogenic differentiation and thus serve an important role in the initiation, development, and progression of bone diseases such as tumors, osteoarthritis and osteoporosis. It has been reported that the lncRNA, maternally expressed gene 3 (MEG3), regulates osteogenic differentiation of multiple MSCs and also acts as a critical mediator in the development of bone formation and associated diseases. In the present review, the proposed mechanisms underlying the roles of MEG3 in osteogenic differentiation and its potential effects on bone diseases are discussed. These discussions may help elucidate the roles of MEG3 in osteogenic differentiation and highlight potential biomarkers and therapeutic targets for the treatment of bone diseases. Contents 1. Introduction 2. Roles of lncRNA MEG3 in osteogenic differentiation 3. Roles of lncRNA MEG3 in bone diseases 4. Conclusion

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“…Current research indicates that MEG3 is involved in tumorigenesis (34)(35)(36)(37). In addition, MEG3 was also found to inhibit prostate cancer progression (38) and breast cancer progression by activating NF-κB and p53 (39); MEG3 inhibits progression of osteosarcoma (40). But so far, the mechanism of action of MEG3 in tumorigenesis is still unclear, especially the regulation of stem cells is rarely reported.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA MEG3 blocks telomerase activity in human liver cancer stem cells epigenetically

Jiang

Wang

Xie

et al. 2020

Preprint

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Background: MEG3 is abnormally down-regulated in most tumors and inhibits tumorigenesis.Methods: Gene infection, Western blotting and tumorigenesis test in vitro and in vivo were performed to analyze the signaling pathway. Results: MEG3 increased the loading of P300 and RNA polymerase II onto the promoter regions of P53. Notably, MEG3 increased the methylation of histone H3 at lysine 27 through increasing the interplay between PRC2 and histone H3. Furthermore, MEG3 inhibited the expression of TERT by increasing the H3K27me3 and decreasing the loading of RNA pol Ⅱ in TERT promoter regions. Moreover, MEG3 inhibit the activity of telomerase by reducing the binding of TERT to TERC competitively. In addition, MEG3 also increased the TERRA through reducing DNA methyltransferase DNMT3b binding to the promoter regions of TERRA competitively. Therefore, the interaction between TERC and TERT was competitively attenuated by increasing the interaction between TERRA and TERT, which inhibited the activity of telomerase in hLCSCs.In particular, MEG3 shortened the length of telomere by blocking the formation of complex maintaining telomere length(POT1-Exo1-TRF2-SNM1B) and decreasing the binding of the complex to telomere competitively, which was caused by increasing the interplay between P53 and HULC in hLCSCs.Strikingly, MEG3 inhibited the growth in vitro and in vivo of hLCSCs by reducing the activity of telomerase and attenuating telomeric repeat binding factor 2(TRF2).Conclusions: our results demonstrated MEG3 inhibits the occurrence of human liver cancer and these findings provide an important insight into the prevention and treatment of human liver cancer.

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Long noncoding RNA MEG3 play an important role in osteosarcoma development through sponging microRNAs

Cited by 20 publications

References 40 publications

Overexpression of FES might inhibit cell proliferation, migration, and invasion of osteosarcoma cells

Overexpression of FES might inhibit cell proliferation, migration, and invasion of osteosarcoma cells

Long non‑coding RNA MEG3 is involved in osteogenic differentiation and bone diseases (Review)

Long noncoding RNA MEG3 blocks telomerase activity in human liver cancer stem cells epigenetically

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