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Epitranscriptomics & Cancer Adaptation : A.David

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Our research work focuses on the contribution of post-transcriptional mechanisms on cancer cell adaptation, in particular RNA epigenetic & translational control.

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Added by lklinares
Group name EquipeLL
Item Type Journal Article
Title Glycogen metabolism is dispensable for tumour progression in clear cell renal cell carcinoma
Creator Xie et al.
Author Hong Xie
Author Jun Song
Author Jason Godfrey
Author Romain Riscal
Author Nicolas Skuli
Author Itzhak Nissim
Author M. Celeste Simon
Abstract Glycogen accumulation is a highly consistent, distinguishable characteristic of clear cell renal cell carcinoma (ccRCC)1. While elevated glycogen pools might be advantageous for ccRCC cells in nutrient-deprived microenvironments to sustain tumour viability, data supporting a biological role for glycogen in ccRCC are lacking. Here, we demonstrate that glycogen metabolism is not required for ccRCC proliferation in vitro nor xenograft tumour growth in vivo. Disruption of glycogen synthesis by CRISPR-mediated knockout of glycogen synthase 1 (GYS1) has no effect on proliferation in multiple cell lines, regardless of glucose concentrations or oxygen levels. Similarly, prevention of glycogen breakdown by deletion or pharmacological inhibition of glycogen phosphorylase B (PYGB) and L (PYGL) has no impact on cell viability under any condition tested. Lastly, in vivo xenograft experiments using the ccRCC cell line, UMRC2, reveal no substantial changes in tumour size or volume when glycogen metabolism is altered, largely mimicking the phenotype of our in vitro observations. Our findings suggest that glycogen build-up in established ccRCC tumour cells is likely to be a secondary, and apparently dispensable, consequence of constitutively active hypoxia-inducible factor 1-alpha (HIF-1?) signalling.
Publication Nature Metabolism
Volume 3
Issue 3
Pages 327-336
Date 2021-03
Journal Abbr Nat Metab
Language eng
DOI 10.1038/s42255-021-00367-x
ISSN 2522-5812
Library Catalog PubMed
Extra PMID: 33758423 PMCID: PMC7995639
Tags Carcinoma, Renal Cell, Cell Proliferation, clinic, Disease Progression, Gene Expression Regulation, Neoplastic, Glycogen, Glycogen Synthase, Humans, Kidney Neoplasms, Tumor Microenvironment
Date Added 2024/12/03 - 09:12:56
Date Modified 2024/12/03 - 09:12:56
Notes and Attachments PubMed entry (Attachment)
Version acceptée (Attachment)


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