miR-382 Inhibits Osteosarcoma Metastasis and Relapse by Targeting Y Box-Binding Protein 1

Xu, Meng; Jin, Hua; Xu, Cheng-Xiong; Sun, Bo; Song, Zhigang; Bi, Wenzhi; Wang, Yan

doi:10.1038/mt.2014.197

Cited by 88 publications

(98 citation statements)

References 50 publications

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“…The inhibition of miR-382 upregulated E-cadherin expression and altered the cellular phenotypes in diabetic kidneys [26, 29]. In cancer, miR-382 was shown to suppress osteosarcoma metastasis by targeting YB-1 oncogene [30, 31]. The regulatory roles of hsa-miR-382-5p in tendon biology remain unexplored and in our study, downregulation of hsa-miR-382-5p and was found to hold a strong correlation with increased ECM damage in Group 1 tendons suggesting its role in maintaining tendon ECM integrity.…”

Section: Discussionmentioning

confidence: 99%

MicroRNAs Associated with Shoulder Tendon Matrisome Disorganization in Glenohumeral Arthritis

et al. 2016

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The extracellular matrix (ECM) provides core support which is essential for the cell and tissue architectural development. The role of ECM in many pathological conditions has been well established and ECM-related abnormalities leading to serious consequences have been identified. Though much has been explored in regards to the role of ECM in soft tissue associated pathologies, very little is known about its role in inflammatory disorders in tendon. In this study, we performed microRNA (miRNA) expression analysis in the long head of the human shoulder biceps tendon to identify key genes whose expression was altered during inflammation in patients with glenohumeral arthritis. We identified differential regulation of matrix metalloproteinases (MMPs) that could be critical in collagen type replacement during tendinopathy. The miRNA profiling showed consistent results between the groups and revealed significant changes in the expression of seven different miRNAs in the inflamed tendons. Interestingly, all of these seven miRNAs were previously reported to have either a direct or indirect role in regulating the ECM organization in other pathological disorders. In addition, these miRNAs were also found to alter the expression levels of MMPs, which are the key matrix degrading enzymes associated with ECM-related abnormalities and pathologies. To our knowledge, this is the first report which identifies specific miRNAs associated with inflammation and the matrix reorganization in the tendons. Furthermore, the findings also support the potential role of these miRNAs in altering the collagen type ratio in the tendons during inflammation which is accompanied with differential expression of MMPs.

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Section: Discussionmentioning

confidence: 99%

MicroRNAs Associated with Shoulder Tendon Matrisome Disorganization in Glenohumeral Arthritis

et al. 2016

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“…The lower wells contained the same medium supplemented with 10% serum. After 24 hr, the cells that had migrated to the lower side of the chamber were fixed, dyed, and counted as previously described 14 . For the osteosphere formation assay, 1,000 cells were seeded in six-well ultra-low cluster plates (Corning) and cultured for 8 days.…”

Section: Methodsmentioning

confidence: 99%

miR-135b Stimulates Osteosarcoma Recurrence and Lung Metastasis via Notch and Wnt/β-Catenin Signaling

Jin

Luo

Wang

et al. 2017

Molecular Therapy - Nucleic Acids

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Cancer stem cells (CSCs) play an important role in osteosarcoma (OS) metastasis and recurrence, and both Wnt/β-catenin and Notch signaling are essential for the development of the biological traits of CSCs. However, the mechanism that underlies the simultaneous hyperactivation of both Wnt/β-catenin and Notch signaling in OS remains unclear. Here, we report that expression of miR-135b correlates with the overall and recurrence-free survival of OS patients, and that miR-135b has an activating effect on both Wnt/β-catenin and Notch signaling. The overexpression of miR-135b simultaneously targets multiple negative regulators of the Wnt/β-catenin and Notch signaling pathways, including glycogen synthase kinase-3 beta (GSK3β), casein kinase 1a (CK1α), and ten-eleven translocation 3 (TET3). Therefore, upregulated miR-135b promotes CSC traits, lung metastasis, and tumor recurrence in OS. Notably, antagonizing miR-135b potently inhibits OS lung metastasis, cancer cell stemness, CSC-induced tumor formation, and recurrence in xenograft animal models. These findings suggest that miR-135b mediates the constitutive activation of Wnt/β-catenin and Notch signaling, and that the inhibition of miR-135b is a novel strategy to inhibit tumor metastasis and prevent CSC-induced recurrence in OS.

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“…MicroRNA-133a is demonstrated to be decreased in OS and acts as a tumor suppressor by targeting Bcl-xL and Mcl-1 [11]. Downregulation of miR-382 encourages OS metastasis and relapse by targeting Y Boxbinding protein 1 [12]. The miR-183 expression is remarkably associated with OS metastasis by regulating Ezrin [13].…”

Section: Introductionmentioning

confidence: 96%

MicroRNA-26b inhibits metastasis of osteosarcoma via targeting CTGF and Smad1

et al. 2015

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Downregulation of miR-26b has been found in various cancers, but it has never been investigated in osteosarcoma. In this study, we demonstrated downregulation of miR-26b in osteosarcoma tissues, negatively correlated with the expression of connective tissue growth factor (CTGF) and Smad1. Luciferase reporter assay confirmed the interaction of miR-26b with the 3' untranslated regions (UTRs) of CTGF and Smad1. Transfection of miR-26b in osteosarcoma cells suppressed the expression of CTGF and Smad1, suggesting CTGF and Smad1 as direct targets of miR-26b. Overexpression of miR-26b inhibited the migration of osteosarcoma cells, which was reversed by overexpression of CTGF or Smad1. Knockdown of CTGF by small interfering RNA (siRNA) interference blocked the activation of Smad1, ERK1/2, and MMP2, which was opposite to the overexpression of CTGF. Differently, Smad1 did not significantly affect CTGF level, but mediated ERK1/2 phosphorylation and MMP2 activation. Furthermore, miR-26b inhibited lung metastasis of osteosarcoma in vivo. Our data indicated that downregulation of miR-26b in osteosarcoma elevated the levels of CTGF and Smad1, facilitating osteosarcoma metastasis.

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miR-382 Inhibits Osteosarcoma Metastasis and Relapse by Targeting Y Box-Binding Protein 1

Cited by 88 publications

References 50 publications

MicroRNAs Associated with Shoulder Tendon Matrisome Disorganization in Glenohumeral Arthritis

MicroRNAs Associated with Shoulder Tendon Matrisome Disorganization in Glenohumeral Arthritis

miR-135b Stimulates Osteosarcoma Recurrence and Lung Metastasis via Notch and Wnt/β-Catenin Signaling

MicroRNA-26b inhibits metastasis of osteosarcoma via targeting CTGF and Smad1

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