Down-Regulation of the miR-25 and miR-30d Contributes to the Development of Anaplastic Thyroid Carcinoma Targeting the Polycomb Protein EZH2

Esposito, Francesco; Tornincasa, Mara; Pallante, Pierlorenzo; Federico, Antonella; Borbone, Eleonora; Pierantoni, Giovanna Maria; Fusco, Alfredo

doi:10.1210/jc.2011-3068

Cited by 101 publications

(82 citation statements)

References 33 publications

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“…These data suggest that the Ezh2 gene plays a role in promoting the proliferation of glioma cells. Consistent with our findings, previous studies have also shown that the Ezh2 gene promotes the proliferation of lung (18), breast (9), thyroid (19), colon (20), ovarian (21), and pancreatic cancer cells (22). Therefore, we concluded that the Ezh2 gene plays an important role in the regulation of the proliferation of glioma cells.…”

Section: Discussionsupporting

confidence: 92%

Downregulation of Ezh2 expression by RNA interference induces cell cycle arrest in the G0/G1 phase and apoptosis in U87 human glioma cells

Zhang¹,

Wang²,

Chang³

et al. 2012

Oncology Reports

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Abstract. The Ezh2 gene is an important member of the polycomb-group (PcG) family. As a newly identified oncogene, the expression of Ezh2 has been shown to be significantly increased in prostate cancer, breast cancer, renal cell carcinoma and hepatic cancer; however, a role for Ezh2 in the occurrence of glioma has not yet been reported. In this study, we found that the Ezh2 gene is highly expressed in U87 human glioma cells. Using RNA interference, we demonstrated that the downregulation of Ezh2 expression in U87 human glioma cells resulted in apoptosis and a cell cycle arrest in the G0/G1 phase. In addition, we found that silencing of the Ezh2 gene altered the mitochondrial membrane potential and promoted the release of cytochrome c from the mitochondria. Furthermore, the reduced expression of Ezh2 altered the Bax and Bcl-2 protein levels and led to the activation of caspase 9 and 3. These results indicate that the apoptosis induced in U87 human glioma cells by the silencing of the Ezh2 gene is related to the mitochondrial pathway.

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Section: Discussionsupporting

confidence: 92%

Downregulation of Ezh2 expression by RNA interference induces cell cycle arrest in the G0/G1 phase and apoptosis in U87 human glioma cells

Zhang¹,

Wang²,

Chang³

et al. 2012

Oncology Reports

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“…Cisplatin sensitivity was increased by overexpression of miR-451 in lung cancer cells (41). Another downregulated miRNA, miR-25, may function as a tumor suppressor that inhibits cell proliferation and migration by targeting Smad 7 in colon cancer (44) and EZH2 in anaplastic thyroid carcinoma (45). Finally, studies have suggested a tumor suppressor role for miR-139-5p, which is downregulated in various types of cancer, including endometrial serous adenocarcinoma (46), breast carcinoma (47), glioblastoma (48), bladder cancer (49), basal cell carcinoma (50) and esophageal squamous cell carcinoma (51).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA screening identifies circulating microRNAs as potential biomarkers for osteosarcoma

Li¹,

Zhang²,

Liu³

et al. 2015

Oncology Letters

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Abstract. MicroRNAs (miRNAs) are a family of small non-protein coding RNAs, which regulate the expression of a wide variety of genes at the post-transcriptional level to control numerous biological and pathological processes. Various circulating miRNAs have been identified as potential diagnostic and prognostic biomarkers in multiple types of cancer and disease. The aim of the present study was to identify potential miRNA biomarkers for the early diagnosis and relapse prediction of osteosarcoma (OS). miRNA profiling was performed on serum from patients with osteosarcoma and healthy controls. All putative miRNAs were verified by reverse transcription-quantitative polymerase chain reaction analysis of 20 pre-therapeutic OS patients and 20 healthy individuals. The expression of miR-106a-5p, miR16-5p, miR-20a-5p, miR-425-5p, miR451a, miR-25-3p and miR139-5p was demonstrated to be downregulated in the serum of OS patients when compared with that of the healthy controls. Receiver-operating characteristic curve analyses indicated that these 7 miRNAs may be used as diagnostic biomarkers with the ability to discriminate between the healthy cohort and patients with OS. These results provide novel insights into the use of miRNAs in early blood screening for OS.

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“…Several miRNA negatively regulate EZH2 expression, for example, miRNA-101, miRNA-26a, miR-29, and miR-214 negatively regulate EZH2 during various differentiation processes. 56 Furthermore, downregulation of miRNA is frequently associated with abnormally elevated levels of EZH2 in cancer; for instance, the downregulation of miR-25 and miR30d is involved in thyroid carcinoma 57 , let-7 in prostate cancer, 58 miR-98 and miR-214 in esophageal squamous cell carcinoma, miR26a and miR-29 in rhabdomyosarcoma. 59,60 Post-translational modifications of EZH2 PRC2 activity can be regulated by post-translational modifications that are able to control the recruitment of target genes and/or its catalytic activity.…”

Section: Transcriptional Regulation Of Prc2mentioning

confidence: 99%

Roles of enhancer of zeste homolog 2: From skeletal muscle differentiation to rhabdomyosarcoma carcinogenesis

Marchesi

Giordano

Bagella³

2014

Cell Cycle

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Down-Regulation of the miR-25 and miR-30d Contributes to the Development of Anaplastic Thyroid Carcinoma Targeting the Polycomb Protein EZH2

Abstract: The down-regulation of miR-25 and miR-30d could contribute to the process of thyroid cancer progression, leading to the development of anaplastic carcinomas targeting EZH2 mRNA.

Cited by 101 publications

References 33 publications

Downregulation of Ezh2 expression by RNA interference induces cell cycle arrest in the G0/G1 phase and apoptosis in U87 human glioma cells

Downregulation of Ezh2 expression by RNA interference induces cell cycle arrest in the G0/G1 phase and apoptosis in U87 human glioma cells

MicroRNA screening identifies circulating microRNAs as potential biomarkers for osteosarcoma

Roles of enhancer of zeste homolog 2: From skeletal muscle differentiation to rhabdomyosarcoma carcinogenesis

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