MiR-155 Promotes Uveal Melanoma Cell Proliferation and Invasion by Regulating NDFIP1 Expression

Peng, Jing; Liu, Honglei; Liu, Cuihong

doi:10.1177/1533034617737923

Cited by 46 publications

(49 citation statements)

References 33 publications

(35 reference statements)

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“…More and more evidence shows that miRNAs are dysregulated in various tumors, including melanoma. For instance, Peng et al (8) showed that miR-155 promotes uveal melanoma cell proliferation and invasion by regulating NDFIP1 expression. Liu et al (9) reported that miRNA-675 inhibits cell proliferation and invasion in melanoma by directly targeting metadherin.…”

Section: Introductionmentioning

confidence: 99%

miR‑30a‑5p inhibits the proliferation, migration and invasion of melanoma cells by targeting SOX4

Liu

Sun

et al. 2018

Mol Med Report

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MicroRNA (miR)‑30a‑5p has been reported to suppress the progression of hepatocellular cancer, renal cell carcinoma, oral cancer and gastric cancer. However, whether miR‑30a‑5p is involved in the regulation of melanoma remains unclear. The present study revealed that miR‑30a‑5p was downregulated in melanoma tissues and cell lines. Overexpression of miR‑30a‑5p significantly inhibited the proliferation, migration and invasion of melanoma cells in vitro. In addition, ectopic expression of miR‑30a‑5p delayed tumor growth in vivo. In terms of mechanism, miR‑30a‑5p targeted sex determining region Y‑box 4 (SOX4) and impeded the expression of SOX4 in melanoma cells. In addition, SOX4 was upregulated in melanoma tissues and cell lines when compared with normal tissues or cells. Furthermore, overexpression of SOX4 significantly rescued the proliferation, migration and invasion of melanoma cells transfected with miR‑30a‑5p mimics. Taken together, the results of the present study demonstrated that miR‑30a‑5p suppressed the proliferation, migration and invasion of melanoma cells in SOX4‑dependent manner.

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Section: Introductionmentioning

confidence: 99%

miR‑30a‑5p inhibits the proliferation, migration and invasion of melanoma cells by targeting SOX4

Liu

Sun

et al. 2018

Mol Med Report

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“…A relatively high levels of miR-155 was detected in B16F10-released exosomes compared with exosomes extracted from B16 cells. Previous studies indicated that overexpression of miR-155 can promote melanoma cell proliferation and invasion [ 37 ]. However, the effects of overexpression of miR-155 on melanoma angiogenesis have not been reported.…”

Section: Discussionmentioning

confidence: 99%

Melanoma cell-secreted exosomal miR-155-5p induce proangiogenic switch of cancer-associated fibroblasts via SOCS1/JAK2/STAT3 signaling pathway

Zhou

Yan

Huang

et al. 2018

J Exp Clin Cancer Res

217

179

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BackgroundCancer-associated fibroblasts (CAFs) have been widely reported to promote tumor angiogenesis. However, the underlying mechanisms of the proangiogenic switch of CAFs remain poorly understood. This study aims to clarify the mechanisms underlying the proangiogenic switch of CAFs.MethodsNIH/3T3 cells were treated with B16 and B16F10-derived exosomes. Then the CAFs markers and proangiogenic factors were detected by RT-PCR and Western blot. CCK-8 assay, transwell migration assay, tube formation assay, and in vivo Matrigel plug assay were conducted to determine the proangiogenic capability of CAFs. Western blot and AG490 were used to investigate the role of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in the proangiogenic switch of CAFs. Bioinformatics analysis, luciferase reporter assay, microRNA mimic and inhibitor, and xenograft models were used to investigate the role of mmu-miR-155-5p (miR-155) in the proangiogenic switch of CAFs.ResultsIn this study, we show that melanoma cell-secreted exosomes can induce reprogramming of fibroblasts into CAFs and that exosomal miR-155 can trigger the proangiogenic switch of CAFs. Mechanistically exosomal miR-155 can be delivered into fibroblasts and promote the expression of proangiogenic factors, including vascular endothelial growth factor A (VEGFa), fibroblast growth factor 2 (FGF2), and matrix metalloproteinase 9 (MMP9), by directly targeting suppressor of cytokine signaling 1 (SOCS1). Downregulation of SOCS1 activates JAK2/STAT3 signaling pathway and elevates the expression levels of VEGFa, FGF2, and MMP9 in fibroblasts. Treatment with exosomes containing overexpressed miR-155 can promote angiogenesis, and the reduction of miR-155 in melanoma cell-secreted exosomes alleviates angiogenesis in vitro and in vivo.ConclusionsThese results demonstrate that by promoting the expression of proangiogenic factors in recipient fibroblasts via SOCS1/JAK2/STAT3 signaling pathway, melanoma cell-secreted exosomal miR-155 can induce the proangiogenic switch of CAFs. Although tumor angiogenesis is modulated by various factors, exosomal miR-155 may be a potential target for controlling melanoma angiogenesis and used to set up novel strategies to treat melanoma.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0911-3) contains supplementary material, which is available to authorized users.

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“…Other oncogenic miRNAs include miR-155 [85], miR-20a [86], and miR-216a-5p that targets the hexokinase 2 (HK 2 ) gene involved in cell metabolism [87]. Interestingly, two oncogenic miRNAs have been shown to target PTEN in UM, namely miR-454 [88] and miR-367 [89].…”

Section: Mirna As Oncogenes In Ummentioning

confidence: 99%

MicroRNAs and Uveal Melanoma: Understanding the Diverse Role of These Small Molecular Regulators

Aughton

Kalirai

Coupland

2020

IJMS

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Uveal melanoma (UM) is a rare tumour of the eye, characterised by a high propensity to metastasise in half of all patients, most frequently to the liver. Although there are effective treatment options for the primary tumour, once metastasis has occurred prognosis is poor, with overall survival limited to months. Currently, there are no effective treatments for metastatic UM, despite the tumour having a well-defined signalling pathway to which many therapies have been directed. In an effort to develop novel treatment approaches, understanding the role of other signalling molecules, such as microRNAs, is fundamental. MicroRNAs (miRNAs) are small non-coding RNA molecules involved in posttranscriptional gene regulation, resulting in reduced target gene expression and subsequent protein translation. In UM, several dysregulated miRNAs have been proposed to play a functional role in disease progression, whereas others have been put forward as clinical biomarkers of high-risk disease following isolation from blood, plasma and exosomes. Most recently, analyses of large datasets have identified promising prognostic miRNA signatures and panels. This review navigates the plethora of aberrant miRNAs disclosed so far in UM, and maps these to signalling pathways, which could be targeted in future therapies for the disseminated disease.

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MiR-155 Promotes Uveal Melanoma Cell Proliferation and Invasion by Regulating NDFIP1 Expression

Cited by 46 publications

References 33 publications

miR‑30a‑5p inhibits the proliferation, migration and invasion of melanoma cells by targeting SOX4

miR‑30a‑5p inhibits the proliferation, migration and invasion of melanoma cells by targeting SOX4

Melanoma cell-secreted exosomal miR-155-5p induce proangiogenic switch of cancer-associated fibroblasts via SOCS1/JAK2/STAT3 signaling pathway

MicroRNAs and Uveal Melanoma: Understanding the Diverse Role of These Small Molecular Regulators

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