Expression and regulatory roles of lncRNAs in G-CIMP-low vs G-CIMP-high Glioma: an in-silico analysis

Noushmehr, Houtan; Brodie, Chaya; Poisson, Laila

doi:10.1186/s12967-021-02844-z

Cited by 6 publications

(3 citation statements)

References 35 publications

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“…To clarify the heterogeneity of PCGI methylation-driven genes in TCGA-GBM tumor samples, we performed the consensus cluster method to cluster the samples based on the similarity of PCGI methylation-driven genes expression signature ( Datta et al, 2021 ). It is worth noting that all samples were likely categorized into three clusters named ClusterA, ClusterB, and ClusterC because the interference between clusters can be minimized when K = 3 was selected ( Figure 1C and Supplementary Figures S1C–L ) ( Gong et al, 2020 ).…”

Section: Resultsmentioning

confidence: 99%

Regulatory pattern of abnormal promoter CpG island methylation in the glioblastoma multiforme classification

Wang

Zhao²,

Wang³

et al. 2022

Front. Genet.

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Glioblastoma (GBM) is characterized by extensive genetic and phenotypic heterogeneity. However, it remains unexplored primarily how CpG island methylation abnormalities in promoter mediate glioblastoma typing. First, we presented a multi-omics scale map between glioblastoma sample clusters constructed based on promoter CpG island (PCGI) methylation-driven genes, using datasets including methylation profiles, expression profiles, and single-cell sequencing data from multiple highly annotated public clinical cohorts. Second, we identified differences in the tumor microenvironment between the two glioblastoma sample clusters and resolved key signaling pathways between cell clusters at the single-cell level based on comprehensive comparative analyses to investigate the reasons for survival differences between two of these clusters. Finally, we developed a diagnostic map and a prediction model for glioblastoma, and compared theoretical differences of drug sensitivity between two glioblastoma sample clusters. In summary, this study established a classification system for dissecting promoter CpG island methylation heterogeneity in glioblastoma and provides a new perspective for the diagnosis and treatment of glioblastoma.

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Section: Resultsmentioning

confidence: 99%

Regulatory pattern of abnormal promoter CpG island methylation in the glioblastoma multiforme classification

Wang

Zhao²,

Wang³

et al. 2022

Front. Genet.

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“…Correlation analysis between the candidate miRNAs and FAM83A identified hsa-miR-129-5p as the most adaptive upstream miRNA of FAM83A which suppresses its expression. Previous studies showed that hsa−miR−129−5p plays a vital regulatory role in glioma (34) and is involved in chemoresistance in ovarian cancer cells (35). However, few studies have focused on the potential mechanism of hsa−miR −129−5p in regulating target genes and tumorigenesis of PC.…”

Section: Discussionmentioning

confidence: 99%

ncRNA-mediated upregulation of FAM83A is associated with poor prognosis and immune infiltration in pancreatic cancer

Zou

Wang

et al. 2023

Front. Endocrinol.

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IntroductionMalignant pancreatic cancer has poor long-term survival. Increasing evidence shows that FAM83A (family with sequence similarity 83 member A) plays a vital role in tumorigenesis and malignant progression in some human cancer types. The present study explored the potential mechanism of FAM83A in improving the prognosis of pancreatic cancer patients.MethodsTranscriptomic and clinical data from patients were obtained from The Cancer Genome Atlas while FAM83A expression was measured in tumorous pancreatic tissue compared with normal controls by quantitative real-time PCR and immunohistochemistry.ResultsFAM83A is a vital prognostic indicator and potential oncogene in pancreatic cancer via pan-cancer analysis. In silico analysis revealed that AL049555.1/hsa-miR-129-5p axis was the pivotal upstream ncRNA- mediated pathway of FAM83A in pancreatic cancer. Furthermore, FAM83A expression was related to immune cell infiltration through vital immune-related genes including programmed cell death 1 (PDCD1), and tumorigenesis through common mutation genes including KRAS protooncogene GTPase (KRAS), and SMAD family member 4 (SMAD4). In summary, ncRNA-mediated upregulation of FAM83A is associated with poor long-term survival and immune cell infiltration in pancreatic cancer.DiscussionFAM83A may be used as a novel survival-related and immune-related biomarker. This information suggests that FAM83A may be a novel therapeutic target for combined or individual treatment for patients with pancreatic cancer.

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“…HCG11 is elevated in patients with atherosclerosis [25]. What is more, HCG11 has been reported to be involved in the expression and regulation of glioma, a malignant tumour of the central nervous system in adults [9]. However, the role of HCG11 in CI/R injury remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through microRNA miR-381-3p to regulate tumour protein p53

Gao¹,

Gao²,

Du³

et al. 2022

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Introduction: Long non-coding RNA (LncRNA) plays a critical role in cerebral ischemia-reperfusion (CI/R) injury. The purpose of the current research was to investigate the regulatory role of the LncRNA human leukocyte antigen complex group 11 (HCG11) in CI/R injury and explore its potential mechanism. Material and methods: The rat middle cerebral artery occlusion (MCAO) model was established to simulate CI/R injury in vivo. mRNA levels of HCG11, microRNA (miR)-381-3p, tumour protein p53, and neuro-inflammatory factors were detected by quantitative reverse transcription PCR (RT-qPCR). Bederson score and Longa score were assessed for neurological deficits. Triphenyl tetrazolium chloride (TTC) staining was used to examine the cerebral infarct volume. What is more, oxidative stress was evaluated by the commercial kit. Finally, the relationship between HCG11, miR-381-3p, and p53 was verified by a dual-luciferase reporter assay. Results: HCG11 was elevated in MCAO rats. And it competitively bound miR-381-3p and down-regulated the expression of p53. Inhibition of HCG11 inhibited cerebral infarct volume and neurological deficits in MCAO rats, and inhibited the secretion of neuro-inflammation and the over-activation of oxidative stress, exerting the protective effect of CI/R injury. However, inhibition of miR-381-3p in rats significantly weakened the protective effect of depression of HCG11 in MCAO rats, resulting in increased cerebral infarction volume and neurological deficits, elevated neuro-inflammatory secretion, and oxidative stress activation. Conclusions: The present research shows that LncRNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through miR-381-3p to regulate p53.

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Expression and regulatory roles of lncRNAs in G-CIMP-low vs G-CIMP-high Glioma: an in-silico analysis

Cited by 6 publications

References 35 publications

Regulatory pattern of abnormal promoter CpG island methylation in the glioblastoma multiforme classification

Regulatory pattern of abnormal promoter CpG island methylation in the glioblastoma multiforme classification

ncRNA-mediated upregulation of FAM83A is associated with poor prognosis and immune infiltration in pancreatic cancer

Long non-coding RNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through microRNA miR-381-3p to regulate tumour protein p53

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