MicroRNA-1/206 Targets c-Met and Inhibits Rhabdomyosarcoma Development

Yan, Dongsheng; Dong, Xiang Da; Chen, Xiaoyan; Wang, Lihua; Lu, Chun-Jing; Wang, Jiao; Qu, Jia; Tu, Lili

doi:10.1074/jbc.m109.020511

Cited by 245 publications

(262 citation statements)

References 25 publications

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“…The mRNA of MET, whose 3'-UTR contains miR-206-binding sites, was previously demonstrated to be a specific target of miR-206 in rhabdomyosarcoma (24). In the present study, it was observed that MET was downregulated significantly at both the mRNA and protein levels ( Fig.…”

Section: Overexpression Of Mir-206 Downregulated the Expression Of Mesupporting

confidence: 65%

MicroRNA-206 inhibits the viability and migration of human lung adenocarcinoma cells partly by targeting MET

et al. 2016

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Abstract. MicroRNA (miRNA)-based targeting in cancer has emerged as a potential therapeutic strategy. miR-206 has recently been implicated in cancer. However, the role and molecular mechanism of miR-206 in lung adenocarcinoma are still unclear. The present study revealed that miR-206 was downregulated in human lung adenocarcinoma tissues. Overexpression of miR-206 in human lung adenocarcinoma-derived cells significantly inhibited cell viability and migration. Further experiments indicated that the overexpression of miR-206 decreased the expression of MET at the messenger RNA and protein levels via direct targeting of MET in a 3'-untranslated region-dependent manner. The knockdown of MET by small interfering RNA partly led to a phenocopy effect of miR-206. In conclusion, the present study identified miR-206 as a potential tumor suppressor of lung adenocarcinoma that exerts its functions, in part, by negative regulation of MET.

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Section: Overexpression Of Mir-206 Downregulated the Expression Of Mesupporting

confidence: 65%

MicroRNA-206 inhibits the viability and migration of human lung adenocarcinoma cells partly by targeting MET

et al. 2016

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“…To further explore the relevance of this finding, we compared our findings with other published works on miRNA expression profile in rhabdomyosarcoma and compiled expression data for miR-1, miR-133a, miR-133b, and miR-206 from ten studies that compared rhabdomyosarcoma with normal skeletal muscle (Supplementary Table 2). [9][10][11][12][13][24][25][26][27][28] The prior studies showed underexpression of miR-1 and miR-133a (if examined) in all nine studies and variable expression of miR-133b and miR-206 across the comparisons of rhabdomyosarcoma to normal skeletal muscle. The underexpression of the myomiRs miR-1, miR-133a, and miR-206 in well-differentiated liposarcoma was validated using qRT-PCR (Figures 2b and d).…”

Section: Qrt-pcr Analysismentioning

confidence: 92%

“…9 Re-expression of miR-29 in xenograft tumors and rhabdomyosarcoma cell lines led to inhibition of tumor proliferation as well as stimulation of myogenic differentiation. Similarly, the muscle-specific miRNA (myomiR), miR-206, is downregulated in rhabdomyosarcoma, [11][12][13][14] and investigators found that re-expression of miR-206 in xenografted tumors stopped proliferation and stimulated myogenic differentiation. 11 The MET protooncogene has been implicated as a target of miR-206 and was indeed silenced with miR-206 re-expression.…”

mentioning

confidence: 99%

“…11 The MET protooncogene has been implicated as a target of miR-206 and was indeed silenced with miR-206 re-expression. 11,12 Up until recently, most studies on miRNAs in sarcoma have utilized frozen specimens and have used tissue obtained from different patients as normal controls. Given the variability in miRNA expression between different individuals, [15][16][17] this methodology may lead to inaccurate results.…”

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confidence: 99%

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A selective screening platform reveals unique global expression patterns of microRNAs in a cohort of human soft-tissue sarcomas

Balkhi

Ladner

et al. 2016

Laboratory Investigation

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Sarcomas are malignant heterogenous tumors of mesenchymal derivation. Emerging data suggest that miRNA might have a causal role in sarcomagenesis. Herein, we used a selective miRNA screening platform to study the comparative global miRNA expression signatures in a cohort of human sarcomas with the caveat that comparisons between tumor and non-tumor cells were performed from the same patients using formalin-fixed paraffin-embedded tissue. Five histologic types were examined that included: myxoid liposarcoma, well-differentiated liposarcoma, dedifferentiated liposarcoma, pleomorphic rhabdomyosarcoma, and synovial sarcoma. In addition, soft-tissue lipomas and normal fat were included as a separate set of controls for the lipogenic tumors. Clustering analysis showed a distinct global difference in expression patterns between the normal and sarcoma tissues. Expression signatures in an unsupervised hierarchical clustering analysis revealed tight clustering in synovial and myxoid liposarcomas, and the least clustering was observed in the pleomorphic rhabdomyosarcoma subtype. MiR-145 showed underexpression in pleomorphic rhabdomyosarcoma, well-differentiated liposarcoma, and synovial sarcoma. Unexpectedly, we found that a set of muscle-specific microRNAs (miRNAs; myomiRs): miR-133, miR-1, and miR-206 was significantly underexpressed in well-differentiated liposarcoma and synovial sarcoma, suggesting that they may function as tumor suppressors as described in muscle-relevant rhabdomyosarcomas. In addition, a tight linear progression of miRNA expression was identified from normal fat to dedifferentiated liposarcoma. These results suggest that miRNA expression profiles could elucidate classes of miRNAs that may elicit tumor-relevant activities in specific sarcoma subtypes. Sarcomas are rare malignant heterogeneous tumors of mesenchymal derivation with over 50 histologic types described. 1 The pathogenesis and biology of many of the different histologic subtypes remain poorly understood. Recent progress in understanding the biology of sarcomas has identified distinct molecular and pathologic entities within these heterogeneous groups of tumors that have paved the way for development of targeted therapies. There are emerging data that seem to suggest that miRNA might be a driver in sarcomagenesis with potential therapeutic implications. microRNAs (miRNAs) are non-coding strands of RNA of 22 nucleotides in length that regulate the expression of genes involved in processes such as development, differentiation, cell proliferation, metabolism, cell death, viral infection, and cancer. 2,3 They have a broad effect through base pairing with mRNA at their 3′ untranslated region to inhibit translation or to target the mRNA for degradation. Bioinformatics predictions have shown that miRNAs regulatẽ 30% of mammalian protein-coding genes. Their role in the molecular biology of cancers is well-established partly

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“…MicroRNAs (miRNAs) help to regulate many cellular processes, including cell-fate determination, proliferation, differentiation and apoptosis, by refining gene expression at the transcriptional or post-transcriptional level [22][23][24][25][26] . Particularly, knocking out Dicer (an RNase III endonuclease responsible for miRNA maturation) in mouse skeletal muscle with MyoD-Cre or Pax7-Cre showed that many miRNAs are required for muscle development and SC functions 27,28 .…”

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confidence: 99%

MicroRNA-431 accelerates muscle regeneration and ameliorates muscular dystrophy by targeting Pax7 in mice

Zhai

et al. 2015

Nat Commun

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Skeletal muscle stem cells, called satellite cells, are a quiescent heterogeneous population. Their heterogeneity is influenced by Pax7, a well-defined transcriptional regulator of satellite cell functions that defines two subpopulations: Pax7 Hi and Pax7 Lo . However, the mechanisms by which these subpopulations are established and maintained during myogenesis are not completely understood. Here we show that miR-431, which is predominantly expressed in the skeletal muscle, mediates satellite cell heterogeneity by fine-tuning Pax7 levels during muscle development and regeneration. In miR-431 transgenic mice, the Pax7 Lo subpopulation is enriched, enhances myogenic differentiation and accelerates muscle regeneration. Notably, miR-431 attenuates the muscular dystrophic phenotype in mdx mice and may be a potential therapeutic target in muscular diseases. miR-431 transgenic mice are a unique genetic model for investigating the cellular features and biological functions of Pax7 Lo satellite cells during muscle development and regeneration.

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MicroRNA-1/206 Targets c-Met and Inhibits Rhabdomyosarcoma Development

Cited by 245 publications

References 25 publications

MicroRNA-206 inhibits the viability and migration of human lung adenocarcinoma cells partly by targeting MET

MicroRNA-206 inhibits the viability and migration of human lung adenocarcinoma cells partly by targeting MET

A selective screening platform reveals unique global expression patterns of microRNAs in a cohort of human soft-tissue sarcomas

MicroRNA-431 accelerates muscle regeneration and ameliorates muscular dystrophy by targeting Pax7 in mice

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