The proteomic landscape of glioma stem-like cells

Lichti, Cheryl F.; Wildburger, Norelle C.; Shavkunov, Alexander S.; Mostovenko, Ekaterina; Liu, Huiling; Sulman, Erik P.; Nilsson, Carol L.

doi:10.1016/j.euprot.2015.06.008

Cited by 12 publications

(8 citation statements)

References 86 publications

(124 reference statements)

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“…To further demonstrate the increased cancer stemness of F3.EGFRviii spheres, expression levels of typical cancer stemness genes were determined using a commercially available PCR array. Several genes, including LIN28A [ 38 ], CD44 [ 39 ], SOX2 [ 40 ], CXCL8 (IL-8) [ 41 ], MYCN [ 42 ], ID1 [ 43 ], and KLF4 [ 44 ], all of which were previously reported to be overexpressed in GSCs, were significantly upregulated in F3.EGFRviii spheres compared with the adherent control cells (Additional file 3 : Fig. S2F and G).…”

Section: Resultsmentioning

confidence: 99%

Role of MEK partner-1 in cancer stemness through MEK/ERK pathway in cancerous neural stem cells, expressing EGFRviii

Kwon

Kim

et al. 2017

Mol Cancer

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BackgroundGlioma stem cells (GSCs) are a major cause of the frequent relapse observed in glioma, due to their high drug resistance and their differentiation potential. Therefore, understanding the molecular mechanisms governing the ‘cancer stemness’ of GSCs will be particularly important for improving the prognosis of glioma patients.MethodsWe previously established cancerous neural stem cells (CNSCs) from immortalized human neural stem cells (F3 cells), using the H-Ras oncogene. In this study, we utilized the EGFRviii mutation, which frequently occurs in brain cancers, to establish another CNSC line (F3.EGFRviii), and characterized its stemness under spheroid culture.ResultsThe F3.EGFRviii cell line was highly tumorigenic in vitro and showed high ERK1/2 activity as well as expression of a variety of genes associated with cancer stemness, such as SOX2 and NANOG, under spheroid culture conditions. Through meta-analysis, PCR super-array, and subsequent biochemical assays, the induction of MEK partner-1 (MP1, encoded by the LAMTOR3 gene) was shown to play an important role in maintaining ERK1/2 activity during the acquisition of cancer stemness under spheroid culture conditions. High expression of this gene was also closely associated with poor prognosis in brain cancer.ConclusionThese data suggest that MP1 contributes to cancer stemness in EGFRviii-expressing glioma cells by driving ERK activity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-017-0703-y) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Role of MEK partner-1 in cancer stemness through MEK/ERK pathway in cancerous neural stem cells, expressing EGFRviii

Kwon

Kim

et al. 2017

Mol Cancer

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“…Sun et al 2018; Hingst et al 2018; Zellner et al 2018; Clemente et al 2018; Lee et al 2018; Adav, Wei, et al 2018; C. Y. Chen et al 2018; Lietzén et al 2018; Jin et al 2018; Klaeger et al 2017; Lawrence et al 2015; Sabrkhany et al 2018; Sathe et al 2019; Adav, Subbaiaih, et al 2018; Nassa et al 2018; Zhao et al 2016; Bereczki et al 2018; Lepper et al 2018; Worzfeld et al 2018; Park et al 2017; Murgia et al 2017; Casanova et al 2017; Cominetti et al 2018; Oller Moreno et al 2018; Sim et al 2019; Papaioannou et al 2019; Tran et al 2018; Fel et al 2019; Koch et al 2019; Brummer et al 2019; Fornecker et al 2019; Lichti et al 2015; Yang et al 2019).…”

Section: Methodsmentioning

confidence: 99%

Massive proteogenomic reanalysis of publicly available proteomic datasets of human tissues in search for protein recoding via adenosine-to-inosine RNA editing

Levitsky

Ivanov

Goncharov³

et al. 2022

Preprint

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The proteogenomic search pipeline developed in this work has been applied for re-analysis of 40 publicly available shotgun proteomic datasets from various human tissues comprising more than 8,000 individual LC-MS/MS runs, of which 5442 .raw data files were processed in total. The scope of this re-analysis was focused on searching for ADAR-mediated RNA editing events, their clustering across samples of different origin, and classification. In total, 33 recoded protein sites were identified in 21 datasets. Of those, 18 sites were detected in at least two datasets representing the core human protein editome. In agreement with prior art works, neural and cancer tissues were found being enriched with recoded proteins. Quantitative analysis indicated that recoding of specific sites did not directly depend on the levels of ADAR enzymes or targeted proteins themselves, rather it was provided by differential and yet undescribed regulation of interaction of enzymes with mRNA. Nine recoding sites conservative between human and rodents were validated by targeted proteomics using stable isotope standards in murine brain cortex and cerebellum, and an additional one was validated in human cerebrospinal fluid. In addition to previous data of the same type from cancer proteomes, we provide a comprehensive catalog of recoding events caused by ADAR RNA editing in the human proteome.

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“…Ribo-seq and mRNA-seq data of respectively GSC2, GSC20, GSC28 and GSC34 were used for analysis. To compare our genes identi ed with ribosome pro ling with proteome data, published mass-spec data 33 was used of GSC2, GSC20, GSC28 and GSC34. In this paper, foldchanges relative to M37 (a mixed control sample containing equal protein from each of the GSC cell lines studied) were used to compare and characterize GSCs.…”

Section: Discussionmentioning

confidence: 99%

The translatome of Glioblastoma multiforme

Cornelissen

Haas

et al. 2022

Preprint

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Background Glioblastoma Multiforme (GBM) is the most common and aggressive brain tumor, containing intrinsic resistance to current therapies leading to poor clinical outcomes. Therefore, understanding the underlying mechanisms of GBM is an urgent medical need. Although radiotherapy contributes significantly to patient survival, GBMs recur typically within the initial radiation target volume, suggesting remaining GBM cells are highly radioresistant. Deregulation of the protein translation mechanism has been shown to contribute to cancer progression by driving translational control of specific mRNA transcripts involved in cancer cell regulation. Methods To identify new potential therapeutic targets for the treatment of GBM we performed ribosome profiling of glioma sphere cultures (GSCs) under normal and radiotherapeutic conditions. Results We found that the global translation of genes matched and overlapped with previously published GBM subtypes, based on the transcriptional level. In addition, we revealed a broad spectrum of open reading frame types in both coding and non-coding regions, including a set of lncRNAs and pseudogenes undergoing active translation. In addition, we identified new mRNA transcripts being translated. Finally, we show that translation of histones is downregulated while splicing factors are intensively translated after irradiation of GSCs. Conclusions Together, our unprecedented GBM riboprofiling provides new insights in real time protein synthesis in GBM under normal and radiotherapeutic conditions which forms a resource for future research and provides potential new targets for therapy.

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The proteomic landscape of glioma stem-like cells

Cited by 12 publications

References 86 publications

Role of MEK partner-1 in cancer stemness through MEK/ERK pathway in cancerous neural stem cells, expressing EGFRviii

Role of MEK partner-1 in cancer stemness through MEK/ERK pathway in cancerous neural stem cells, expressing EGFRviii

Massive proteogenomic reanalysis of publicly available proteomic datasets of human tissues in search for protein recoding via adenosine-to-inosine RNA editing

The translatome of Glioblastoma multiforme

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