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Genome-wide translation patterns in gliomas: An integrative view

期刊

CELLULAR SIGNALLING
卷 79, 期 -, 页码 -

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2020.109883

关键词

Glioma; Glioblastoma; Translatome; Gene expression; Translational control

资金

  1. Fundacno de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2015/15451-3, 2018/17796-6]
  2. Conselho Nacional de Desenvolvimento Cientffico e TecnolOgico (CNPq) [422981/2018-4]
  3. CNPq

向作者/读者索取更多资源

Gliomas, particularly glioblastoma, exhibit deregulation of translational control due to overactivation of signaling pathways such as PI3K/AKT/mTORC1 and Ras/ERK1/2. Transcriptome analysis can provide important insights into gene expression patterns in gliomas.
Gliomas are the most frequent tumors of the central nervous system (CNS) and include the highly malignant glioblastoma (GBM). Characteristically, gliomas have translational control deregulation related to overactivation of signaling pathways such as PI3K/AKT/mTORC1 and Ras/ERK1/2. Thus, mRNA translation appears to play a dominant role in glioma gene expression patterns. The, analysis of genome-wide translated transcripts, together known as the translatome, may reveal important information for understanding gene expression patterns in gliomas. This review provides a brief overview of translational control mechanisms altered in gliomas with a focus on the current knowledge related to the translatomes of glioma cells and murine glioma models. We present an integrative meta-analysis of selected glioma translatome data with the aim of identifying recurrent patterns of gene expression preferentially regulated at the level of translation and obtaining clues regarding the pathological significance of these alterations. Re-analysis of several translatome datasets was performed to compare the translatomes of glioma models with those of their non-tumor counterparts and to document glioma cell responses to radiotherapy and MNK modulation. The role of recurrently altered genes in the context of translational control and tumorigenesis are discussed.

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