Over-expression of the <i>miR-483-3p</i> overcomes the miR-145/TP53 pro-apoptotic loop in hepatocellular carcinoma

Lupini, Laura; Pepe, Felice; Ferracin, Manuela; Braconi, Chiara; Callegari, Elisa; Pagotto, Sara; Spizzo, Riccardo; Zagatti, Barbara; Lanuti, Paola; Fornari, Francesca; Ghasemi, Reza; Mariani-Costantini, Renato; Bolondi, Luigi; Gramantieri, Laura; Calin, George A.; Sabbioni, Silvia; Visone, Rosa; Veronese, Angelo; Negrini, Massimo

doi:10.18632/oncotarget.8913

Cited by 44 publications

(39 citation statements)

References 43 publications

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“…Anti-p21 (MS-891-B Thermo Scientific) Western Blot was performed on cell extracts as described [49] using BT20 cells exposed to 9 × 10 −6 m protein for 4 h. Fold increase of p21 was referred to a β-actin control. Sections were incubated with 10% normal goat serum (NGS) in antibody diluent (1% BSA in 100 × 10 −3 m Tris buffer) and then of 1:100 dilution of anti-p21 antibody (M 7202, Dako, Santa Clara, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Targeting Antitumoral Proteins to Breast Cancer by Local Administration of Functional Inclusion Bodies

Pesarrodona

Jauset²,

Díaz‐Riascos

et al. 2019

Advanced Science

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Two structurally and functionally unrelated proteins, namely Omomyc and p31, are engineered as CD44‐targeted inclusion bodies produced in recombinant bacteria. In this unusual particulate form, both types of protein materials selectively penetrate and kill CD44+ tumor cells in culture, and upon local administration, promote destruction of tumoral tissue in orthotropic mouse models of human breast cancer. These findings support the concept of bacterial inclusion bodies as versatile protein materials suitable for application in chronic diseases that, like cancer, can benefit from a local slow release of therapeutic proteins.

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Section: Methodsmentioning

confidence: 99%

Targeting Antitumoral Proteins to Breast Cancer by Local Administration of Functional Inclusion Bodies

Pesarrodona

Jauset²,

Díaz‐Riascos

et al. 2019

Advanced Science

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“…Interestingly, this study also demonstrated that miR‐483‐5p could promote IGF2 transcription in turn by enhancing the RNA helicase DHX9 associated with the IGF2 transcript. For miR‐483‐3p, it has been reported dysregulated in multiple cancers, implying it could participate in regulating cell functions, such as growth and apoptosis 38, 39…”

Section: Discussionmentioning

confidence: 99%

IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1

Zhi

Zhu

et al. 2018

J Cellular Molecular Medi

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HSCR (Hirschsprung's disease) is a serious congenital defect, and the aetiology of it remains unclear. Many studies have highlighted the significant roles of intronic miRNAs and their host genes in various disease, few was mentioned in HSCR although. In this study, miR‐483‐3p along with its host gene IGF2 (Insulin‐like growth factor 2) was found down‐regulated in 60 HSCR aganglionic colon tissues compared with 60 normal controls. FHL1 (Four and a half LIM domains 1) was determined as a target gene of miR‐483‐3p via dual‐luciferase reporter assay, and its expression was at a higher level in HSCR tissues. Here, we study cell migration and proliferation in human 293T and SH‐SY5Y cell lines by performing Transwell and CCK8 assays. In conclusion, the knockdown of miR‐483‐3p and IGF2 both suppressed cell migration and proliferation, while the loss of FHL1 leads to opposite outcome. Furthermore, miR‐483‐3p mimics could rescue the negative effects on cell proliferation and migration caused by silencing IGF2, while the FHL1 siRNA may inverse the function of miR‐483‐3p inhibitor. This study revealed that miR‐483‐3p derived from IGF2 was associated with Hirschsprung's disease by targeting FHL1 and may provide a new pathway to understand the aetiology of HSCR.

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“…Moreover, SET overexpression was proven to be a common alteration in early-stage CRC, promoting cell migration and EMT in CRC cells (Cristóbal et al, 2019). The miR-145-5p was downregulated in several tumors, including hepatocellular carcinomas, via p53 pathway apoptosis (Lupini et al, 2016). However, the posttranscriptional regulation role of miR-145-5p in CRC through SET has not yet been found.…”

Section: Discussionmentioning

confidence: 99%

Post-Transcriptional Dysregulation of microRNA and Alternative Polyadenylation in Colorectal Cancer

et al. 2020

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Background: Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide. microRNAs (miRNAs) repress gene expression by binding to complementary sequences in the 3' untranslated region (3'UTR) of target mRNAs. Alternative polyadenylation (APA) are relevant to the variability of the 3'UTR of mRNA. However, the posttranscriptional dysregulation of miRNAs and APA in CRC are poorly understood.Method: In this study, we conducted small RNA sequencing to identify differentially expressed miRNAs (DERs) and their target genes. Function analysis on DER-target genes can explain the regulation roles of miRNAs in CRC. The mutual regulation of miRNAs and APA was analyzed by combining miRNA data to 3'UTR alteration using 3' termini of polyadenylated RNAs sequencing (3T-seq) technique, and this was validated using TCGA gene expression data.Results: Our results showed 64 significant differentially expressed miRNAs (DERs) in CRC patients. Their target genes were related to cell adhesion and transcription regulation and were prevailingly involved in the CRC-related pathway. Integrative analysis of the miRNA and APA profile revealed 16 DERs were correlated with 12 polyadenylation factors, and six of them were significantly differently expressed in CRC. We also found four DERs that lost binding sites due to APA and showed a positive correlation between the miRNA and gene expression.Conclusion: Our study found that miRNAs regulated APA by modulating key polyadenylation factors, and several miRNAs lost their suppression on mRNA due to APA. Associating this with gene expression may provide some important clues for a deeper study of posttranscriptional cellular regulation and biomarker research in CRC. Our data provided the first evidence that the interaction between miRNAs and APA associated with gene expression could serve as biomarkers for CRC, suggesting that hsa-miR-133a-Frontiers in Genetics | www.frontiersin.org 3p and MLEC, hsa-miR-145-5p and SET, hsa-miR-1-3p and PPIA, and hsa-miR-378d and YY1 might be novel and potential biomarkers in improving the diagnosis of CRC.

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Over-expression of the miR-483-3p overcomes the miR-145/TP53 pro-apoptotic loop in hepatocellular carcinoma

Cited by 44 publications

References 43 publications

Targeting Antitumoral Proteins to Breast Cancer by Local Administration of Functional Inclusion Bodies

Targeting Antitumoral Proteins to Breast Cancer by Local Administration of Functional Inclusion Bodies

IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1

Post-Transcriptional Dysregulation of microRNA and Alternative Polyadenylation in Colorectal Cancer

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