Sox2 is translationally activated by eukaryotic initiation factor 4E in human glioma-initiating cells

Ge, Yuqing; Zhou, Fengbiao; Chen, Hong; Cui, Chunhong; Liú, Dan; Li, Qiuping; Yang, Zhiyuan; Wu, Guoqiang; Sun, Shuhui; Gu, Jianxin; Wei, Yuanyan; Jiang, Jianhai

doi:10.1016/j.bbrc.2010.06.015

Cited by 33 publications

(25 citation statements)

References 34 publications

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“…Indeed, Myc and Sox2 mRNAs sedimented with heavy polysomes in the Oct4-infected TKO MEFs in comparison to the Oct4-infected p53KO MEFs, whereas there was no difference in the sedimentation of Klf4, Gapdh, and b-actin mRNAs ( Figures 5C and S5A-S5D). These findings are consistent with previous reports demonstrating that the translation of Myc and Sox2 mRNAs is eIF4E dependent (De Benedetti and Graff, 2004;Ge et al, 2010;Stoyanova et al, 2013). Accordingly, the levels of MYC and SOX2 proteins were upregulated in the Oct4-infected TKO MEFs and coincided with the induction of NANOG expression ( Figure 5D).…”

Section: Translation Of Sox2 and Myc Mrnas Is Induced In The Oct4-expsupporting

confidence: 93%

Multifaceted Regulation of Somatic Cell Reprogramming by mRNA Translational Control

et al. 2014

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Translational control plays a pivotal role in the regulation of the pluripotency network in embryonic stem cells, but its effect on reprogramming somatic cells to pluripotency has not been explored. Here, we show that eukaryotic translation initiation factor 4E (eIF4E) binding proteins (4E-BPs), which are translational repressors, have a multifaceted effect on the reprogramming of mouse embryonic fibroblasts (MEFs) into induced pluripotent stem cells (iPSCs). Loss of 4E-BP expression attenuates the induction of iPSCs at least in part through increased translation of p21, a known inhibitor of somatic cell reprogramming. However, MEFs lacking both p53 and 4E-BPs show greatly enhanced reprogramming resulting from a combination of reduced p21 transcription and enhanced translation of endogenous mRNAs such as Sox2 and Myc and can be reprogrammed through the expression of only exogenous Oct4. Thus, 4E-BPs exert both positive and negative effects on reprogramming, highlighting the key role that translational control plays in regulating this process.

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Section: Translation Of Sox2 and Myc Mrnas Is Induced In The Oct4-expsupporting

confidence: 93%

Multifaceted Regulation of Somatic Cell Reprogramming by mRNA Translational Control

et al. 2014

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“…eIF4E overexpression protected cells from tunicamycin-induced cell growth arrest [45]. Our published data has shown that cap binding protein eIF4E activated Sox2 translation in glioma stem-like cells [46]. Based on these finding, we presume that tunicamycin might reduce Sox2 translation through inactivation of translation regulator eIF2 or eIF4E, which should be further investigated.…”

Section: Discussionmentioning

confidence: 97%

ER stress inducer tunicamycin suppresses the self-renewal of glioma-initiating cell partly through inhibiting Sox2 translation

Yang

Liu

et al. 2016

Oncotarget

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Glioma-initiating cells possess tumor-initiating potential and are relatively resistant to conventional chemotherapy and irradiation. Therefore, their elimination is an essential factor for the development of efficient therapy. Here, we report that endoplasmic reticulum (ER) stress inducer tunicamycin inhibits glioma-initiating cell self-renewal as determined by neurosphere formation assay. Moreover, tunicamycin decreases the efficiency of glioma-initiating cell to initiate tumor formation. Although tunicamycin induces glioma-initiating cell apoptosis, apoptosis inhibitor z-VAD-fmk only partly abrogates the reduction in glioma-initiating cell self-renewal induced by tunicamycin. Indeed, tunicamycin reduces the expression of self-renewal regulator Sox2 at translation level. Overexpression of Sox2 obviously abrogates the reduction in glioma-initiating cell self-renewal induced by tunicamycin. Taken together, tunicamycin suppresses the self-renewal and tumorigenic potential of glioma-initiating cell partly through reducing Sox2 translation. This finding provides a cue to potential effective treatment of glioblastoma through controlling stem cells.

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“…The expression of eIF4E is upregulated in several kinds of cancer (Bjornsti & Houghton, 2004). In this study the authors suggest that eIF4E is regulating Sox2 on the protein level but not on the mRNA level and that the eIF4E-Sox2 affiliation could be a new potential therapeutic target (Ge, et al, 2010). An immunotherapy study has been performed by Schmitz et al, who first showed that Sox2 is overexpressed in GBM.…”

Section: The Essence Of Sox2 and Sox21 In Brain Tumoursmentioning

confidence: 79%

“…Yet another study shows that Sox2 is involved in self-renewal in glioma, by overexpressing Sox2 in glioma cells did the number and size of neurospheres increase. In addition there is a correlation between Sox2 expression and eIF4E (eukaryotic initiation factor 4E) in glioma tissue samples (Ge, et al, 2010). eIF4E is a mRNA 5' cap-binding protein, which takes part in regulation of translational initiation (Richter & Sonenberg, 2005).…”

Section: The Essence Of Sox2 and Sox21 In Brain Tumoursmentioning

confidence: 99%

The Role of Sox Transcription Factors in Brain Tumourigenesis

Ferletta¹

2011

Molecular Targets of CNS Tumors

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Sox2 is translationally activated by eukaryotic initiation factor 4E in human glioma-initiating cells

Cited by 33 publications

References 34 publications

Multifaceted Regulation of Somatic Cell Reprogramming by mRNA Translational Control

Multifaceted Regulation of Somatic Cell Reprogramming by mRNA Translational Control

ER stress inducer tunicamycin suppresses the self-renewal of glioma-initiating cell partly through inhibiting Sox2 translation

The Role of Sox Transcription Factors in Brain Tumourigenesis

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