The miR‐139‐5p regulates proliferation of supratentorial paediatric low‐grade gliomas by targeting the PI3K/AKT/mTORC1 signalling

Catanzaro, Giuseppina; Besharat, Zein Mersini; Miele, Evelina; Chiacchiarini, Martina; Pò, Agnese; Carai, Andrea; Marras, Carlo Efisio; Antonelli, Manila; Badiali, Manuela; Raso, Alessandro; Mascelli, Samantha; Schrimpf, Daniel; Stichel, Damian; Tartaglia, Marco; Capper, David; Deimling, Andreas von; Giangaspero, Felice; Mastronuzzi, Angela; Locatelli, Franco; Ferretti, Elisabetta

doi:10.1111/nan.12479

Cited by 36 publications

(35 citation statements)

References 67 publications

(114 reference statements)

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“…Pharmacological inhibition of Vegfa was induced by treating SHH MB CSC cells for 72 h with 10, 20, 40 and 60 ng/ml anti-Vegf (MAB 293, R&D Systems). Synthetic miR-466f-3p (4464066, Thermo Fisher Scientific) or negative control (miRIDIAN CN-001000-01; Dharmacon) were used as previously described ( Catanzaro et al, 2018 ). Cell proliferation was evaluated by trypan blue exclusion assay ( Catanzaro et al, 2018 ).…”

Section: Methodsmentioning

confidence: 99%

“…Synthetic miR-466f-3p (4464066, Thermo Fisher Scientific) or negative control (miRIDIAN CN-001000-01; Dharmacon) were used as previously described ( Catanzaro et al, 2018 ). Cell proliferation was evaluated by trypan blue exclusion assay ( Catanzaro et al, 2018 ). Oncosphere-forming assay of SHH MB CSC was performed as previously described ( Po et al, 2010 ).…”

Section: Methodsmentioning

confidence: 99%

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Low Expression of miR-466f-3p Sustains Epithelial to Mesenchymal Transition in Sonic Hedgehog Medulloblastoma Stem Cells Through Vegfa-Nrp2 Signaling Pathway

et al. 2018

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High-throughput analysis has improved the knowledge of medulloblastoma (MB), the leading cause of cancer related death in children, allowing a better comprehension of the key molecular pathways in MB pathogenesis. However, despite these advances, 30% of patients still die from the disease and survivors face severe long-term side effects. Cancer stem cells (CSCs) represent a subset of cells that not only drive tumorigenesis, but are also one of the main determinants of chemoresistance. Epithelial mesenchymal transition (EMT) is a hallmark of cancer and up to now few data is available in MB. To give insight into the role of the EMT process in maintaining the mesenchymal phenotype of CSCs, we analyzed the expression of EMT related transcripts and microRNAs in these cells. We firstly isolated CSCs from Sonic Hedgehog (SHH) MB derived from Ptch1 heterozygous mice and compared their expression level of EMT-related transcripts and microRNAs with cerebellar NSCs. We identified two molecules linked to SHH and EMT, Vegfa and its receptor Nrp2, over-expressed in SHH MB CSCs. Inhibition of Vegfa showed impairment of cell proliferation and self-renewal ability of CSCs concurrent with an increase of the expression of the EMT gene, E-cadherin, and a decrease of the EMT marker, Vimentin. Moreover, among deregulated microRNAs, we identified miR-466f-3p, a validated inhibitor of both Vegfa and Nrp2. These results allowed us to describe a new EMT molecular network, involving the down-regulation of miR-466f-3p together with the concordant up-regulation of Vegfa and Nrp2, that sustains the mesenchymal phenotype of SHH MB CSCs.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Low Expression of miR-466f-3p Sustains Epithelial to Mesenchymal Transition in Sonic Hedgehog Medulloblastoma Stem Cells Through Vegfa-Nrp2 Signaling Pathway

et al. 2018

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“…MicroRNAs (miRNAs) are 18-25 nucleotide long non-coding RNAs that act as post-transcriptional regulators of gene expression. MiRNA "signatures/profiles" have been reported as specific in several cellular contexts and diseases (Catanzaro, et al, 2018;Catanzaro, et al, 2017;Esquela-Kerscher & Slack, 2006;Iorio & Croce, 2012;Miele, et al, 2013) as well as in response to therapy (Chan, Prado, & Weidhaas, 2011;Gasparri, et al, 2017;Gasparri, et al, 2018;Skinner, et al, 2014). Previous studies reported the aberrant expression of specific miRNAs in MTC tissues, suggesting these miRNAs as candidate biomarkers.…”

Section: J O U R N a L P R E -P R O O Fmentioning

confidence: 99%

Role of tissue and circulating microRNAs and DNA as biomarkers in medullary thyroid cancer

Chiacchiarini

Trocchianesi

Besharat

et al. 2021

Pharmacology & Therapeutics

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…For example, phosphatidylinositol 3-kinase (PI3K), a lipid kinase that regulates the levels of phosphorylated phosphatidylinositol at the plasma membrane and enhances glucose uptake and glycolysis in cancer cell metabolism, is targeted by miR-320, miR-123a, miR-422, miR-506, and miR-136 (127). Catanzaro et al showed evidence that downregulation of miR-139-5p in pediatric low-grade gliomas drives cell proliferation by regulating PI3K/AKT signaling (128). Furthermore, miR-33a/b, targets metabolic enzymes involved in fatty acid metabolism and the AMPK pathway, whereas miR-29b targets amino acid catabolism, which regulates cancer cell metabolism and biogenesis to support tumor growth and proliferation (61, 129-131).…”

Section: Mirnas Regulation Of Transcription Factors and Signaling Patmentioning

confidence: 99%

MicroRNAs in Tumor Cell Metabolism: Roles and Therapeutic Opportunities

et al. 2019

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Dysregulated metabolism is a common feature of cancer cells and is considered a hallmark of cancer. Altered tumor-metabolism confers an adaptive advantage to cancer cells to fulfill the high energetic requirements for the maintenance of high proliferation rates, similarly, reprogramming metabolism confers the ability to grow at low oxygen concentrations and to use alternative carbon sources. These phenomena result from the dysregulated expression of diverse genes, including those encoding microRNAs (miRNAs) which are involved in several metabolic and tumorigenic pathways through its post-transcriptional-regulatory activity. Further, the identification of key actionable altered miRNA has allowed to propose novel targeted therapies to modulated tumor-metabolism. In this review, we discussed the different roles of miRNAs in cancer cell metabolism and novel miRNA-based strategies designed to target the metabolic machinery in human cancer.

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The miR‐139‐5p regulates proliferation of supratentorial paediatric low‐grade gliomas by targeting the PI3K/AKT/mTORC1 signalling

Abstract: These findings provide the first evidence that down-regulation of miR-139-5p in supratentorial pLGG drives cell proliferation by derepressing PI3K/AKT signalling.

Cited by 36 publications

References 67 publications

Low Expression of miR-466f-3p Sustains Epithelial to Mesenchymal Transition in Sonic Hedgehog Medulloblastoma Stem Cells Through Vegfa-Nrp2 Signaling Pathway

Low Expression of miR-466f-3p Sustains Epithelial to Mesenchymal Transition in Sonic Hedgehog Medulloblastoma Stem Cells Through Vegfa-Nrp2 Signaling Pathway

Role of tissue and circulating microRNAs and DNA as biomarkers in medullary thyroid cancer

MicroRNAs in Tumor Cell Metabolism: Roles and Therapeutic Opportunities

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