miR-130b-3p Upregulation Contributes to the Development of Thyroid Adenomas Targeting &lt;b&gt;&lt;i&gt;CCDC6&lt;/i&gt;&lt;/b&gt; Gene

Leone, Vincenza; Langella, Carla; Esposito, Francesco; Martino, Marco De; Decaussin‐Petrucci, Myriam; Chiappetta, Gennaro; Bianco, Antonio

doi:10.1159/000441355

Cited by 12 publications

(7 citation statements)

References 30 publications

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“…For miRNA detection, total RNA from cells or tissues was reverse-transcribed using miScript Reverse Transcription Kit (Qiagen, Hilden, Germany). Real-Time PCR was performed following miScript System Kits (Qiagen, Hilden, Germany) instructions [ 26 ]. Real-Time PCR reactions contained miScript Primer Sets (Qiagen, Hilden, Germany), specific for Mm-mir-483-5p 5′-aagacgggagaagagaagggag -3′, Mm-mir-483-3p 5′-ucacuccuccccucccgucuu-3′, Mm-mir-675-5p 5′-uggugcggaaagggcccacagu-3′, Mm-mir-21-3p 5′-caacagcagucgaugggcuguc-3′, Mm-mir-187-3p 5′-ucgugucuuguguugcagccgg-3′, Mm-mir-214 5′-acagcaggcacagacaggcagu-3′, Mm-mir-761 5′-gcagcagggugaaacugacaca-3′.…”

Section: Methodsmentioning

confidence: 99%

The HMGA1 Pseudogene 7 Induces miR-483 and miR-675 Upregulation by Activating Egr1 through a ceRNA Mechanism

Martino

Palma

Azzariti

et al. 2017

Genes

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Several studies have established that pseudogene mRNAs can work as competing endogenous RNAs and, when deregulated, play a key role in the onset of human neoplasias. Recently, we have isolated two HMGA1 pseudogenes, HMGA1P6 and HMGA1P7. These pseudogenes have a critical role in cancer progression, acting as micro RNA (miRNA) sponges for HMGA1 and other cancer-related genes. HMGA1 pseudogenes were found overexpressed in several human carcinomas, and their expression levels positively correlate with an advanced cancer stage and a poor prognosis. In order to investigate the molecular alterations following HMGA1 pseudogene 7 overexpression, we carried out miRNA sequencing analysis on HMGA1P7 overexpressing mouse embryonic fibroblasts. Intriguingly, the most upregulated miRNAs were miR-483 and miR-675 that have been described as key regulators in cancer progression. Here, we report that HMGA1P7 upregulates miR-483 and miR-675 through a competing endogenous RNA mechanism with Egr1, a transcriptional factor that positively regulates miR-483 and miR-675 expression.

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Section: Methodsmentioning

confidence: 99%

The HMGA1 Pseudogene 7 Induces miR-483 and miR-675 Upregulation by Activating Egr1 through a ceRNA Mechanism

Martino

Palma

Azzariti

et al. 2017

Genes

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“…miR-130b-3p has been shown to have different effects in different cancer types, and functions as an oncogene in thyroid adenomas 23 and epithelial ovarian cancer 39 . miR-130b-3p also acts as a tumor suppressor in breast carcinoma 22 and ovarian cancer 40 .…”

Section: Discussionmentioning

confidence: 99%

“…However, it has been found that miR-130b-3p could directly target the Notch ligand Delta-like 1 (DLL1) and inhibit breast carcinoma cell invasion and migration 22 . It has been suggested that the upregulation of miR-130b-3p contributed to the development of thyroid adenomas by targeting the CCDC6 gene 23 . In a pilot RNA-seq analysis of exosome in the plasma of MB patients (GSE123376), we found exosomal miR-130b-3p was elevated in the plasma of MB patients.…”

Section: Introductionmentioning

confidence: 99%

Exosomal miR-130b-3p targets SIK1 to inhibit medulloblastoma tumorigenesis

et al. 2020

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Exosomes are an important carrier for cell communication. miRNAs in exosomes are potential biomarkers and therapeutic targets in different types of cancer. However, the role of exosomal miRNAs in medulloblastoma (MB) patients is largely unknown. In this study, we reported that there was a higher level of miR-130b-3p in exosomes derived from MB patient plasma compared with exosomes from healthy control plasma. Exosomes from MB patient plasma could transfer miR-130b-3p to an MB cell line and played suppressor roles for cell proliferation. miR-130b-3p suppressed MB tumorigenesis by targeting a previously unknown target, serine/threonine-protein kinase 1 (SIK1), through the p53 signaling pathways. In addition, we found an unreported role of SIK1 in promoting MB tumor growth and an SIK1 inhibitor could inhibit MB cell proliferation. This research provides new insight into the molecular mechanism of MB and may provide a new therapeutic strategy for MB treatment.

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“…In particular, tissue samples were dissociated with homogenizer. For mRNA detection, 1 mg of RNA from each sample was reverse-transcribed using QuantiTech Reverse Transcription kit (Qiagen, Valencia, CA) [24] and then Real-Time PCR was performed by using iQ SybrGreen SuperMix (BioRad, Hercules, CA). qRT-PCR analyses were performed using the following primers:

h CBX7-fw 5’-cgagtatctggtgaagtggaaa-3’

h CBX7 rev 5’-gggggtccaagatgtgct-3’

h KRAS-fw 5’-aggctcaggacttagcaagaa-3’

h KRAS-rev 5’-gaaggcatcatcaacaccct-3’

m KRAS-fw 5’- tgtggatgagtatgaccctacg-3’

m KRAS-rev 5’- ccctcattgcactgtactcct-3’

…”

Section: Methodsmentioning

confidence: 99%

miR-155 is positively regulated by CBX7 in mouse embryonic fibroblasts and colon carcinomas, and targets the KRAS oncogene

et al. 2017

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BackgroundLoss of CBX7 expression has been described in several malignant neoplasias, including human colon and thyroid carcinomas proposing CBX7 as a tumor suppressor gene with a key role in cancer progression. This role is supported from the development of benign and malignant neoplasias in Cbx7 null mice.The aim of our work has been to investigate the mechanisms underlying the CBX7 oncosuppressor activity by analyzing the microRNAs (miRNAs) regulated by CBX7.MethodsThe miRNA expression profiles of the mouse embryonic fibroblasts (MEFs) null for Cbx7 and the wild-type counterpart were analyzed by the miRNACHIP microarray and then validated by qRT-PCR. To asses KRAS as target of miR-155 we evaluated the protein levels after transfection of the synthetic miR-155. Human colon carcinoma samples have been investigated for the expression of CBX7 and miR-155.ResultsTwenty miRNAs were found upregulated and nine, including miR-155, downregulated in cbx7-null MEFS in comparison with the wild-type ones. Then, we focused on miR-155 since several studies have shown its deregulated expression in several human malignancies and, moreover, was the most downregulated miRNA. Subsequently, we searched for miR-155 target genes demonstrating that KRAS protein levels are directly modulated by miR-155. A direct significant correlation (r = 0.6779) between CBX7 and miR-155 expression levels was found in a set of human colon carcinoma tissue samples.ConclusionmiR-155 is positively regulated by CBX7 in MEFs and colon carcinomas, and has KRAS as one of the target genes likely accounting for the anti-apoptotic activity ascribed to miR-155 in some tissue contexts.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-017-3158-z) contains supplementary material, which is available to authorized users.

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miR-130b-3p Upregulation Contributes to the Development of Thyroid Adenomas Targeting <b><i>CCDC6</i></b> Gene

Cited by 12 publications

References 30 publications

The HMGA1 Pseudogene 7 Induces miR-483 and miR-675 Upregulation by Activating Egr1 through a ceRNA Mechanism

The HMGA1 Pseudogene 7 Induces miR-483 and miR-675 Upregulation by Activating Egr1 through a ceRNA Mechanism

Exosomal miR-130b-3p targets SIK1 to inhibit medulloblastoma tumorigenesis

miR-155 is positively regulated by CBX7 in mouse embryonic fibroblasts and colon carcinomas, and targets the KRAS oncogene

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