MicroRNA-1 functions as a potential tumor suppressor in osteosarcoma by targeting Med1 and Med31

Jiang, Cen; Chen, Hua; Shao, Li; Wang, Qiaojie

doi:10.3892/or.2014.3274

Cited by 19 publications

(11 citation statements)

References 32 publications

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“…Overexpression of miR-1 has been shown to suppress cell proliferation in many cancers; the results of this study were consistent with these past studies (14,15,17). Previous studies have reported that miR-1 suppresses proliferation, migration, and invasion by down-regulating MET (11), Med1 and Med31 (18), and VEGFA (19) in osteosarcoma. Although some studies have reported that miR-1 induced cell-cycle arrest in the G 0 -G 1 phase by targeting MET, Med1 and Med31, a detailed analysis of the downstream genes related to the cell cycle has not been fully performed.…”

Section: Discussionsupporting

confidence: 92%

“…Studies have reported that miR-1 suppresses proliferation, migration, and invasion by down-regulating MET (11), Med1 and Med31 (18), and VEGFA (19) in osteosarcoma. Although some studies have reported that miR-1 induces cell cycle arrest, a detailed analysis on downstream genes related to the cell cycle has not been fully performed, and evidence concerning the in vivo function of miR-1 has not been obtained.…”

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confidence: 99%

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MiR-1 Suppresses Proliferation of Osteosarcoma Cells by Up-regulating p21 via PAX3

Fujii

Osaka

Sato

et al. 2018

Cancer Genomics Proteomics

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Background/Aim: miRNA-1(miR-1) is downregulated in various cancer cells including osteosarcoma cells. This study was conducted to analyze the function of miR-1 in osteosarcoma cells. Materials and Methods: miR-1 expression in osteosarcoma cells was evaluated by qRT-PCR. Cell proliferation was evaluated after transfecting miR-1 by WST8 assay and FACS analysis, both in vitro and in vivo. Results: Overexpression of miR-1 suppressed cell proliferation and induced cell-cycle arrest in the G 0-G 1 phase by increasing p21 levels via a p53-independent pathway. Overexpression of miR-1 down-regulated PAX3, a potential p21-regulating gene. Moreover, knockdown of PAX3 suppressed cell proliferation by increasing p21 levels, and induced arrest at the G 0 /G 1 phase. Administration of miR-1 showed an in vivo antitumor effect. Conclusion: Overexpression of miR-1 suppressed cell proliferation and induced arrest in the G 0 /G 1 phase by increasing p21 levels via a p53-independent pathway through PAX3 suppression. These results indicate that miR-1 could be a therapeutic target for osteosarcoma. Osteosarcoma is a primary bone malignancy that usually occurs in the metaphyseal region of long bones in children and adolescents, producing immature osteoids and bones. Previously, amputation of the extremities, concurrent with detection, was the conventional therapy for osteosarcoma and the 5-year survival rate was extremely poor, less than 20%, due to the inability to inhibit pulmonary metastases (1). Recently, the survival rate has increased to 60-80% through the application of combination treatments using surgery and 71 This article is freely accessible online.

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

MiR-1 Suppresses Proliferation of Osteosarcoma Cells by Up-regulating p21 via PAX3

Fujii

Osaka

Sato

et al. 2018

Cancer Genomics Proteomics

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“…The 3′-UTR of MARCKS containing the putative miR-34c-3p binding sequence was amplified by PCR and cloned downstream of the firefly luciferase gene in the pMIR-Report vector (Promega Corporation, Madison, WI, USA) (12). Mutations in the miR-34c-3p seed regions of the MARCKS 3′UTR were generated using the QuikChang Multisite-directed mutagenesis kit (Promega Corporation).…”

Section: Methodsmentioning

confidence: 99%

miR-34c-3p acts as a tumor suppressor gene in osteosarcoma by targeting MARCKS

Liu

Zhi

et al. 2017

Molecular Medicine Reports

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Previous studies have demonstrated that microRNA (miR)-34c-3p is important in human cancer progression. However, the function of miR-34c-3p in osteosarcoma (OS) remains to be elucidated. In the present study, miR-34c-3p level was measured by reverse transcription-quantitative polymerase chain reaction in OS tissues and the associated prognostic value for overall survival was determined. The function of miR-34c-3p was examined in vitro and in vivo. A luciferase reporter assay was used to identify the targets of miR-34c-3p. The results of the present study revealed that miR-34c-3p was downregulated in OS tissues and cell lines, and decreased levels of miR-34c-3p were associated with a high mortality rate in patients with OS. Furthermore, restoration of miR-34c-3p expression reduced cell growth in vitro and suppressed tumorigenesis in vivo. Conversely, inhibition of miR-34c-3p stimulated OS cell growth in vitro and in vivo. Myristoylated alanine-rich protein kinase C substrate (MARCKS) was identified as a direct target of miR-34c-3p and its overexpression partly reversed the suppressive effects of miR-34c-3p. Furthermore, MARCKS was revealed to be upregulated and inversely correlated with miR-34c-3p levels in OS tissues. These data suggested that miR-34c-3p acts as a tumor suppressor via regulation of MARCKS expression in OS progression and miR-34c-3p may be a promising therapeutic target for this type of cancer.

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“…Indeed, in a screen for target genes, several miRs have been shown to regulate the expression of Mediator components in an embryonic stem cell line (Davis et al, 2012). Additionally, miR-146, miR-1, and miR-205 were shown to bind and regulate MED1 expression in spermatogonia, cancer cells, prostate cells, and trophoblasts, respectively (Hulf et al, 2013; Huszar and Payne, 2013; Jiang et al, 2014; Mouillet et al, 2010). Because MED1 seems to be regulated by multiple miRs, perhaps in a cell-specific manner, it will be important to determine the endogenous role of MED1 in these cell types.…”

Section: Questions For the Futurementioning

confidence: 99%

Muscle as a “Mediator” of Systemic Metabolism

2015

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Skeletal and cardiac muscles play key roles in the regulation of systemic energy homeostasis and display remarkable plasticity in their metabolic responses to caloric availability and physical activity. In this Perspective we discuss recent studies highlighting transcriptional mechanisms that govern systemic metabolism by striated muscles. We focus on the participation of the Mediator complex in this process, and suggest that tissue-specific regulation of Mediator subunits impacts metabolic homeostasis.

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MicroRNA-1 functions as a potential tumor suppressor in osteosarcoma by targeting Med1 and Med31

Cited by 19 publications

References 32 publications

MiR-1 Suppresses Proliferation of Osteosarcoma Cells by Up-regulating p21 via PAX3

MiR-1 Suppresses Proliferation of Osteosarcoma Cells by Up-regulating p21 via PAX3

miR-34c-3p acts as a tumor suppressor gene in osteosarcoma by targeting MARCKS

Muscle as a “Mediator” of Systemic Metabolism

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