An integrative analysis of DNA methylation in osteosarcoma

Xu, Jie; Deng, Li; Cai, Zhiqing; Zhang, Yingbin; Huang, Yulin; Su, Baohua; Ma, Ruofan

doi:10.1016/j.jbo.2017.05.001

Cited by 14 publications

(11 citation statements)

References 42 publications

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“…[ 41 , 42 ] Moreover, cellular growth and differentiation are key processes for carcinoma development and progression. The findings in our study are consistent with recently reported results, [ 43 ] which show that neuroactive ligand-receptor interaction and the PPAR signaling pathway are highly associated with osteosarcoma.…”

Section: Discussionsupporting

confidence: 94%

A panel of eight mRNA signatures improves prognosis prediction of osteosarcoma patients

Zhan

Lin

et al. 2021

Medicine

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Genetic alterations are vital to the progression of osteosarcoma carcinoma. The present study investigated a panel of gene signatures that could evaluate prognosis in osteosarcoma based on data from the Therapeutically Applicable Research To Generate Effective Treatments initiative. Osteosarcoma messenger RNA (mRNA) profiles and clinical data were downloaded from the therapeutically applicable research to generate effective treatments database. Patients with osteosarcoma were divided into two groups based on findings at diagnosis: with and without metastasis. Differentially expressed mRNAs were compared and analyzed between groups. Univariate and multivariate Cox regression analyses identified a set of eight mRNAs with the ability to classify patients into high-risk and low-risk groups with significantly different overall survival times. Further analysis indicated that the eight-mRNA signature was an independent prognostic factor after adjusting for other clinical factors. Receiver operating characteristic curve analysis demonstrated a good performance of the eight-mRNA signature. Further, the biological processes and signaling pathways of the eight-mRNA signature were reviewed using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes resources. Finally, the results of the TCGA analysis were verified by other cohorts from Gene Expression Omnibus database. The identification of an eight-mRNA signature not only provides a prognostic biomarker of osteosarcoma but also offers the potential of novel therapeutic targets for its treatment.

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Section: Discussionsupporting

confidence: 94%

A panel of eight mRNA signatures improves prognosis prediction of osteosarcoma patients

Zhan

Lin

et al. 2021

Medicine

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“…Their potential targeting genes were then clearly shown to us. Among these potential targeting genes, many have been reported to participate in the process of OS, such as cell adhesion molecule 1 (CADM1) [ 18 ], early B cell factor 2 (EBF2) [ 19 ], MAX interactor 1 (MXI1) [ 20 ], and nemo-like kinase (NLK) [ 21 ]. It indicated that these differentially expressed miRNAs may play critical regulating roles in the progression of OS.…”

Section: Discussionmentioning

confidence: 99%

Potential Regulatory Effects of miR-182-3p in Osteosarcoma via Targeting EBF2

Chen

et al. 2019

BioMed Research International

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Osteosarcoma (OS) is one of the most common primary malignant bone tumors in adolescents with a high mortality rate. MicroRNA (miRNA) is a kind of noncoding RNAs and has been proved to participate in many physiological processes. Many miRNAs have been reported to act as function regulators in OS. In our study, the miRNA and gene expression profiles of OS were downloaded from GEO Datasets and the differential expression analysis was performed using GEO2R. 58 up- and 126 downregulated miRNAs were found. In the three OS gene profiles, 125 up- and 27 downregulated genes were found to be differentially expressed in at least two profiles. The miRNA-mRNA networks were constructed to predict the potential target genes of 10 most up- and downregulated miRNA. Venn analysis was used to detect the coexpressed differentially expressed genes (DEGs). EBF2, one of the upregulated DEGs, was also a potential target gene of miR-182-3p. Knockdown and overexpression of miR-182-3p resulted in overexpression and downexpression of EBF2 separately. Luciferase reporter gene experiment further verified the binding site of miR-182-3p and EBF2. CCK8 assay showed that miR-182-3p knockdown can further enhance the proliferation activity of OS cells, while overexpressing miR-182-3p can inhibit the proliferation activity of OS cells. Our research indicated that downexpression of miR-182-3p in OS cells results in overexpression of EBF2 and promotes the progression of OS.

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“…In the PPI network, the MAXI interactor signals transducer 1 (MXI1), the transcription activator STAT3 and the T-cell acute lymphocytic leukemia 1 (TAL1) had the highest degree of hypermethylation. These genes were identified as being associated with cancer and were hypermethylated in OS cells (80).…”

Section: Role Of Epigenetic Mechanismsmentioning

confidence: 99%

Biology and pathogenesis of human osteosarcoma (Review)

Azevedo¹,

Fernandes

et al. 2019

Oncol Lett

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Osteosarcoma (OS) is a bone tumor of mesenchymal origin, most frequently occurring during the rapid growth phase of long bones, and usually located in the epiphyseal growth plates of the femur or the tibia. Its most common feature is genome disorganization, aneuploidy with chromosomal alterations, deregulation of tumor suppressor genes and of the cell cycle, and an absence of DNA repair. This suggests the involvement of surveillance failures, DNA repair or apoptosis control during osteogenesis, allowing the survival of cells which have undergone alterations during differentiation. Epigenetic events, including DNA methylation, histone modifications, nucleosome remodeling and expression of non-coding RNAs have been identified as possible risk factors for the tumor. It has been reported that p53 target genes or those genes that have their activity modulated by p53, in addition to other tumor suppressor genes, are silenced in OS-derived cell lines by hypermethylation of their promoters. In osteogenesis, osteoblasts are formed from pluripotent mesenchymal cells, with potential for self-renewal, proliferation and differentiation into various cell types. This involves complex signaling pathways and multiple factors. Any disturbance in this process can cause deregulation of the differentiation and proliferation of these cells, leading to the malignant phenotype. Therefore, the origin of OS seems to be multifactorial, involving the deregulation of differentiation of mesenchymal cells and tumor suppressor genes, activation of oncogenes, epigenetic events and the production of cytokines. Contents 1. Introduction 2. Biology of human OS 3. Role of differentiation of mesenchymal stem cells 4. Role of DNA changes 5. Role of deregulating the expression of tumor suppressor genes 6. Regulation of oncogene expression 7. Role of epigenetic mechanisms 8. Role of non-coding RNAs 9. Role of cytokines 10. Conclusion

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An integrative analysis of DNA methylation in osteosarcoma

Cited by 14 publications

References 42 publications

A panel of eight mRNA signatures improves prognosis prediction of osteosarcoma patients

A panel of eight mRNA signatures improves prognosis prediction of osteosarcoma patients

Potential Regulatory Effects of miR-182-3p in Osteosarcoma via Targeting EBF2

Biology and pathogenesis of human osteosarcoma (Review)

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