MiR-1 Is a Tumor Suppressor in Thyroid Carcinogenesis Targeting CCND2, CXCR4, and SDF-1α

Leone, Vincenza; D'Angelo, Daniela; Rubio, Ileana G.S.; Freitas, Paula Mussnich de; Federico, Antonio; Colamaio, Marianna; Pallante, Pierlorenzo; Medeiros‐Neto, Geraldo; Fusco, Alfredo

doi:10.1210/jc.2011-0345

Cited by 100 publications

(73 citation statements)

References 35 publications

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“…The data presented here emphasize the dominance of SRC as a miR-1 target and determinant of bone metastatic activity, even though a variety of other miR-1 targets have been described (22,38,39). Additionally, miR-23b was recently described as targeting SRC and AKT in prostate cancer, and it is reasonable to anticipate that miR-1 and miR-23b both contribute to regulating SRC levels (41).…”

Section: Discussionmentioning

confidence: 60%

“…On the other hand, miR-1 has been shown to target several different gene transcripts (Fig. 3B and C) (22,38,39). Having demonstrated that ectopic pre-miR-1 expression decreased SRC expression and the development of bone metastasis, we asked whether reconstitution of SRC levels in miR-1 cells would be sufficient to restore bone metastatic activity.…”

Section: Resultsmentioning

confidence: 99%

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Loss of Androgen-Regulated MicroRNA 1 Activates SRC and Promotes Prostate Cancer Bone Metastasis

Liu

Yin

Barrett

et al. 2015

Molecular and Cellular Biology

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Bone metastasis is the hallmark of progressive and castration-resistant prostate cancers. MicroRNA 1 (miR-1) levels are decreased in clinical samples of primary prostate cancer and further reduced in metastases. SRC has been implicated as a critical factor in bone metastasis, and here we show that SRC is a direct target of miR-1. In prostate cancer patient samples, miR-1 levels are inversely correlated with SRC expression and a SRC-dependent gene signature. Ectopic miR-1 expression inhibited extracellular signal-regulated kinase (ERK) signaling and bone metastasis in a xenograft model. In contrast, SRC overexpression was sufficient to reconstitute bone metastasis and ERK signaling in cells expressing high levels of miR-1. Androgen receptor (AR) activity, defined by an AR output signature, is low in a portion of castration-resistant prostate cancer. We show that AR binds to the miR-1-2 regulatory region and regulates miR-1 transcription. Patients with low miR-1 levels displayed correlated low canonical AR gene signatures. Our data support the existence of an AR-miR-1-SRC regulatory network. We propose that loss of miR-1 is one mechanistic link between low canonical AR output and SRC-promoted metastatic phenotypes.

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Section: Discussionmentioning

confidence: 60%

Section: Resultsmentioning

confidence: 99%

Loss of Androgen-Regulated MicroRNA 1 Activates SRC and Promotes Prostate Cancer Bone Metastasis

Liu

Yin

Barrett

et al. 2015

Molecular and Cellular Biology

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“…In addition, our findings indicated that miR-1-3p functions as tumor suppressors in bladder cancer for its effects on the inhibition of proliferation, migration and invasion. Similarly, Leone et al found that miR-1-3p acted as a tumor-suppressed miRNA [16,17].…”

Section: Discussionmentioning

confidence: 92%

miR-1-3p Contributes to Cell Proliferation and Invasion by Targeting Glutaminase in Bladder Cancer Cells

Zhang

Wang

Mao

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increasing evidence showed that miR-1-3p plays a major role in malignant tumor progression. However, the specific biological function of miR-1-3p in bladder cancer is yet unknown. Methods: The expression levels of miR-1-3p in bladder cancer tissues and cell lines were examined by qRT-PCR. Bisulfite sequencing PCR was used for DNA methylation analysis. The target of miR-1-3p was validated by a dual luciferase reporter assay, and the effects of miR-1-3p on phenotypic changes in bladder cancer cells were investigated in vitro and in vivo. Results: The expression of miR-1-3p in bladder cancer cells was downregulated as compared to normal SV-HUC-1 cells. Also, the expression of miR-1-3p was significantly lower in bladder cancer tissues than the corresponding non-cancerous tissues. The methylation status of CpG islands was involved in the regulation of miR-1-3p expression. miR-1-3p inhibited the bladder cancer cell proliferation, migration, and invasion by directly targeting the 3’-UTR of glutaminase. It also exerted an anti-tumor effect by negatively regulating the glutaminase in a xenograft mouse model. Furthermore, GLS depletion resulted in the prolonged expression of γH2AX. Conclusion: Taken together, these results demonstrated that miR-1-3p acts as a tumor suppressor via regulation of glutaminase expression in bladder cancer progression, and miR-1-3p might represent a novel therapeutic target for the treatment of bladder cancer.

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“…Sheu et al (2010) showed a significant difference of the expression of miR-146b between PTCs and other benign thyroid lesions, such as multinodular goitre (MNG) and FA with foldchanges up to 90. Moreover, four different studies (He et al, 2005;Ricarte-Filho et al, 2009;Leone et al, 2011;Xiong et al, 2011) identified down-regulation of miRNAs in PTC in comparison to normal thyroid tissue. The different miRNA expression profiles in PTCs are shown in Table 1.…”

Section: Mirna Expression Profiles In Papillary Thyroid Carcinomas (Pmentioning

confidence: 99%

Deregulation of microRNA expression in thyroid tumors

Yuan

Yang

Zheng

2014

J. Zhejiang Univ. Sci. B

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MicroRNAs (miRNAs or miRs) are endogenous non-coding RNAs that negatively regulate gene expression by binding to the 3' non-coding regions of target mRNAs, resulting in their cleavage or blocking their translation. miRNAs may have an impact on cell differentiation, proliferation, and survival, and their deregulation can be inclined to diseases and cancers, including thyroid tumors. The purpose of this review is to summarize the existing findings of deregulated miRNAs in different types of thyroid tumors and to exhibit their potential target genes, especially to demonstrate those involved in tumor invasion and metastasis. In addition, new findings of circulating miRNA expression profiles, single nucleotide polymorphism (SNP) in thyroid tumors, and the correlation of somatic mutations with deregulated miRNA expression in thyroid tumors were all included in this review.

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MiR-1 Is a Tumor Suppressor in Thyroid Carcinogenesis Targeting CCND2, CXCR4, and SDF-1α

Abstract: These results indicate the involvement of miR-1 in thyroid cell proliferation and migration, validating a role of miR-1 down-regulation in thyroid carcinogenesis.

Cited by 100 publications

References 35 publications

Loss of Androgen-Regulated MicroRNA 1 Activates SRC and Promotes Prostate Cancer Bone Metastasis

Loss of Androgen-Regulated MicroRNA 1 Activates SRC and Promotes Prostate Cancer Bone Metastasis

miR-1-3p Contributes to Cell Proliferation and Invasion by Targeting Glutaminase in Bladder Cancer Cells

Deregulation of microRNA expression in thyroid tumors

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