Targeting SNHG3/miR-186-5p reverses the increased m6A level caused by platinum treatment through regulating METTL3 in esophageal cancer

Zhang, Mingxin; Bai, Man; Wang, Li; Lü, Ning; Wang, Jia; Yan, Rong; Cui, Manli; Yan, Honglin; Zhang, Lingmin

doi:10.1186/s12935-021-01747-9

Cited by 22 publications

(21 citation statements)

References 26 publications

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“…Indeed, we found that the m 6 A level was much lower in patients than in HCs, demonstrating that m 6 A modification is very important in the process of NMOSD. In addition, Zhang found that altering m 6 A levels might be a novel way for improving the efficacy of platinum in cancer treatment ( Zhang et al, 2021a ), and Zhao reported that m 6 A regulation could influence the progression of lung adenocarcinoma ( Zhao and Xie, 2021 ). We hypothesized that increasing the level of m 6 A might relieve the symptoms of NMOSD, but further studies are needed to confirm this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis of N6-Methyladenosine (m6A) Methylation in Neuromyelitis Optica Spectrum Disorders

Hong

Ding

et al. 2021

Front. Genet.

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Background: N6-Methyladenosine (m6A) methylation is the most prevalent internal posttranscriptional modification on mammalian mRNA. But its role in neuromyelitis optica spectrum disorders (NMOSD) is not known.Aims: To explore the mechanism of m6A in NMOSD patients.Methods: This study assessed the m6A methylation levels in blood from two groups: NMOSD patients and healthy controls. Methylated RNA immunoprecipitation Sequencing (MeRIP-seq) and RNA-seq were performed to assess differences in m6A methylation between NMOSD patients and healthy controls. Ultra-high performance liquid chromatography coupled with triple quadruple mass spectrometry (UPLC-QQQ-MS) method was performed to check m6A level. Differential m6A methylation genes were validated by MeRIP-qPCR.Results: Compared with that in the control group, the total m6A level was decreased in the NMOSD group. Genes with upregulated methylation were primarily enriched in processes associated with RNA splicing, mRNA processing, and innate immune response, while genes with downregulated methylation were enriched in processes associated with the regulation of transcription, DNA-templating, and the positive regulation of I-kappa B kinase/NF-kappa B signalling.Conclusion: These findings demonstrate that differential m6A methylation may act on functional genes to regulate immune homeostasis in NMOSD.

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Section: Discussionmentioning

confidence: 99%

Comprehensive Analysis of N6-Methyladenosine (m6A) Methylation in Neuromyelitis Optica Spectrum Disorders

Hong

Ding

et al. 2021

Front. Genet.

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“…SNHG3 has been identified as a tumorpromoting lncRNA in various cancers. [33][34][35][36] Wu et al 33 found that SNHG3 was upregulated in HCC and could promote cell proliferation, migration, and invasion. Zhang et al 37 found that SNHG3 could induce epithelial-mesenchymal transition and sorafenib resistance in HCC.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, a recent study revealed that SNHG3 could epigenetically regulate its neighboring MED18 gene methylation by binding to EZH2 and inhibiting its expression in gastric cancer. 38 Besides, Zhang et al 34 found that the increased expression of SNHG3 induced by the platinum treatment could regulate the m 6 A level by targeting METTL3 in esophageal cancer. These findings indicated that the important role of SNHG3 in epigenetic regulation of cancer progression and resistance.…”

Section: Discussionmentioning

confidence: 99%

Prognostic Role and Potential Mechanisms of N6-methyladenosine-related Long Noncoding RNAs in Hepatocellular Carcinoma

Dai¹,

Li²,

Ye³

et al. 2021

J Clin Transl Hepatol

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Background and Aims:Numerous studies have explored the important role of N6-methyladenosine (m 6 A) in cancer. Nonetheless, the interaction between m 6 A and long noncoding RNAs (lncRNAs) is poorly investigated. Herein, we systematically analyzed the role and prognostic value of m 6 A-related lncRNAs in hepatocellular carcinoma (HCC). Methods: The m 6 A-related lncRNAs were identified based on the correlation coefficients with m 6 A-related genes in HCC from The Cancer Genome Atlas. Subsequently, a novel risk score model was determined using the least absolute shrinkage and selection operator Cox regression analyses. Univariate and multivariate Cox analyses were used to identify independent prognostic factors for overall survival (OS) of HCC; thereafter, a prognostic nomogram was constructed. Results: A total of 259 lncRNAs showed significant correlations with m 6 A in HCC, while 29 lncRNAs had prognostic significance. Further, six critical m 6 A-related lncRNAs (NRAV, SNHG3, KDM4A-AS1, AC074117.1, AC025176.1, and AL031985.3) were screened out to construct a novel risk score model which classified HCC patients into high-and low-risk groups. Survival analyses revealed that patients in the high-risk group exhibited worse OS, both in the training and validation groups. The risk score was also identified as an independent prognostic factor of OS, and a nomogram was established and verified with superior prediction capacity. Besides, the risk score significantly correlated with the expression of immune checkpoint genes and immune subtypes. Conclusions: These findings indicated the significant role of m 6 A-related lncRNAs in HCC and the potential application of the novel risk score model for prognostic prediction.

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“…It can promote tumorigeneses by epigenetically suppressing MED18 through recruiting EZH2 to methylate the MED18 neighboring region in gastric cancer (29). Recently, in a study, lncRNA SNHG3 has been shown that elevated the m6A level by binding tomiR-186-5p to increase METTL3 expression in the ESCA cells (30).…”

Section: Kaplan-meier Survival Analysis Of Differentially Expressedmentioning

confidence: 99%

Long Non-Coding RNAs Roles in Tumorigenesis of Esophageal Carcinoma

Talebi

Kargar

Jafarinia

et al. 2022

Preprint

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Background:Esophageal carcinoma (ESCA) is one of the most common types of cancer. ESCA is accounted for the sixth leading cause of cancer-related deaths globally. The majority of the patients are diagnosed at late stages of ESCA, with distance metastasis and/or chemoresistance, which lead to a poor prognosis. Previous studies demonstrated lncRNA presentation and roles in ESCA cells and patients tissue. It has been proposed that lncRNAs can be considered as a new prognostic and diagnostic biomarker in ESCA. This study comprehensively explored the interaction of lncRNAs with miRNAs and mRNAs of TCGA database and proposed novel promising biomarker with favorable diagnostic and prognostic values. Methods: The public data of RNA-seq, miR-seq and related clinical data were downloaded from TCGA database. Differential expression analysis was conducted by “limma” in R. GO and KEGG signaling pathway were used for enrichments. STRING database was used for PPI analysis. CE-network was constructed by STAR database in R. Kaplan-Meier survival analysis (log-rank test) and ROC curve analysis to indicate the biomarkers' diagnostic and prognostic values.Results: Differentially expressed data illustrated that 1332 mRNA including 610 upregulated and 722 down-regulated were differentially expressed in ESCA.The GO and KEGG pathway analysis showed that the differentially expressed mRNAs were enriched in critical biological processes. The PPI showed that IGFBP5, ACAN, ADAMTS12, MMP13, and CDH2 were the important PPI hubs. The ceRNA network data demonstrated critical lncRNAs including TMEM16B-AS1, AC093010.3, SNHG3, and PVT1 which have an essential role in ESCA development.The data revealed that the lncRNA WDFY3-AS2, AC108449.2,DLEU2, AC007128.1, and AP003356.1 are potential diagnostic prognostic biomarker in the ESCA patients. Conclusion: Altogether, in our study, we demonstrated lncRNA, miRNA, and mRNA interaction and mentioned regulatory networks, which can be considered as a therapeutic option in ESCA. In addition, we proposed potential diagnostic and prognostic biomarkers for the patients.

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Targeting SNHG3/miR-186-5p reverses the increased m6A level caused by platinum treatment through regulating METTL3 in esophageal cancer

Cited by 22 publications

References 26 publications

Comprehensive Analysis of N6-Methyladenosine (m6A) Methylation in Neuromyelitis Optica Spectrum Disorders

Comprehensive Analysis of N6-Methyladenosine (m6A) Methylation in Neuromyelitis Optica Spectrum Disorders

Prognostic Role and Potential Mechanisms of N6-methyladenosine-related Long Noncoding RNAs in Hepatocellular Carcinoma

Long Non-Coding RNAs Roles in Tumorigenesis of Esophageal Carcinoma

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