Anti-oncogenic MicroRNA-203 Induces Senescence by Targeting E2F3 Protein in Human Melanoma Cells

Noguchi, Shunsuke; Mori, Takashi; Otsuka, Yusami; Yamada, Nami; Yasui, Yuki; Iwasaki, Junya; Kumazaki, Minami; Maruo, Keishi; Akao, Yukihiro

doi:10.1074/jbc.m111.325027

Cited by 103 publications

(78 citation statements)

References 37 publications

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“…Our analysis confirmed the previous report of miR-193b downregulation in metastatic melanoma [49]. In addition, downregulation of miR-203, miR-200a, miR-200c, miR-205 was previously reported in several melanoma cell lines [50][51][52]. Our data reveal that the loss of expression in these miRNAs occurs predominantly in metastatic melanomas compared with primary.…”

Section: Mirna Profiling Of Primary and Metastatic Melanoma Tumorssupporting

confidence: 92%

Scan_Tcga Tools for Integrated Epigenomic and Transcriptomic Analysis of Tumor Subgroups

et al. 2016

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Aim:The Cancer Genome Atlas contains multiple levels of genomic data (mutation, gene expression, DNA methylation, copy number variation) for 33 cancer types for almost 11,000 patients. However, a dearth of appropriate software tools makes it difficult for bench scientists to use these data effectively. Materials & methods: Here, we present a suite of flexible, fast and command line-based scripts that will allow retrieval and analysis of DNA methylation (tool: scan_tcga_methylation.awk), mRNA (tool: scan_tcga_mRNA.awk) and miRNA expression (tool: scan_tcga_miRNAs.awk) from cancer genome atlas network level 3 data. Results: We demonstrate the utility of these tools by analyzing DNA methylation and mRNA expression signatures of 60 frequently deregulated cancer genes and also of 30 miRNAs in primary (n = 102) and metastatic melanoma patients (n = 367). Conclusion: Our analysis illustrates the validity of the scan_tcga tools and reveals the epigenomic signatures and importance of identifying smaller patient subgroups with distinct molecular profiles.

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Section: Mirna Profiling Of Primary and Metastatic Melanoma Tumorssupporting

confidence: 92%

Scan_Tcga Tools for Integrated Epigenomic and Transcriptomic Analysis of Tumor Subgroups

et al. 2016

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“…p63 was shown to be directly targeted by miR-203 in mouse skin epithelial cells (50). In several types of human cancer cells, ABCE1, Abl1, and E2F3 were shown to be directly targeted by miR-203 (33,35,36,68). In this study, we found that miR-203 also targets p63 in RMS cells (Fig.…”

Section: Mir-203 Exerts Tumor-suppressive Effects In Rms Cells-supporting

confidence: 56%

miR-203, a Tumor Suppressor Frequently Down-regulated by Promoter Hypermethylation in Rhabdomyosarcoma

Diao

Guo

Jiang

et al. 2014

Journal of Biological Chemistry

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Background: Rhabdomyosarcoma (RMS) is a pediatric tumor that expresses several muscle-specific proteins with poor terminal differentiation. Results: miR-203 was frequently down-regulated in RMS, and its re-expression in RMS cells inhibited their growth and migration and promoted terminal differentiation. Conclusion: miR-203 is a tumor suppressor down-regulated in RMS. Significance: miR-203 can serve as a potential target for therapeutic treatment of RMS.

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“…It can also target Hakai and inhibit the growth of human colon adenocarcinoma (28). Additionally, those genes involved in the regulation of cell proliferation, apoptosis, cell cycle progression, migration and invasion, are also the targets of miR-203, including Robo1, Kif5b, E2F3, LASP1, ASAP1, PKCα, BIRC5, Bmi-1 and DeltaNp63 (23)(24)(25)(26)(29)(30)(31)(32)(33). Whether these miR-203 targets are also involved in the development and progression of NB remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-203 inhibits the malignant progression of neuroblastoma by targeting Sam68

Zhao

Tian

et al. 2015

Molecular Medicine Reports

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Abstract. Neuroblastoma (NB) is the most common solid extracranial tumor in children. However, the molecular mechanism of NB remains to be elucidated. In the present study, reverse transcription quantitative polymerase chain reaction data demonstrated that the expression of Sam68 was significantly upregulated in NB tissues compared with their matched adjacent normal tissues. Furthermore, it was revealed that reduced expression of miR-203 and increased expression of Sam68 co-existed in NB tissues. Knockdown of Sam68 reduced the proliferation, migration and invasion of human SK-N-SH and SH-SY5Y NB cells. Similarly, overexpression of miR-203 also inhibited the proliferation, migration and invasion of these two cell lines. It was further demonstrated that the protein expression level of Sam68 was negatively mediated by miR-203 in the SK-N-SH and SH-SY5Y NB cells. Additionally, data from a dual luciferase reporter assay confirmed that miR-203 directly targeted Sam68 by binding to its 3'-untranslated region. In conclusion, the present study suggested for the first time, to the best of our knowledge, that the aberrant downregulation of miR-203 may contribute to the aberrant upregulation of Sam68 in NB and that miR-203 has an inhibitory role in malignant progression of NB by targeting Sam68. The present study provided evidence to support miR-203/Sam68 as a novel diagnostic or therapeutic targets for NB.

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Anti-oncogenic MicroRNA-203 Induces Senescence by Targeting E2F3 Protein in Human Melanoma Cells

Cited by 103 publications

References 37 publications

Scan_Tcga Tools for Integrated Epigenomic and Transcriptomic Analysis of Tumor Subgroups

Scan_Tcga Tools for Integrated Epigenomic and Transcriptomic Analysis of Tumor Subgroups

miR-203, a Tumor Suppressor Frequently Down-regulated by Promoter Hypermethylation in Rhabdomyosarcoma

MicroRNA-203 inhibits the malignant progression of neuroblastoma by targeting Sam68

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