Thioredoxin post-transcriptional regulation by H19 provides a new function to mRNA-like non-coding RNA

Lottin, Séverine; Vercoutter‐Edouart, Anne‐Sophie; Adriaenssens, Éric; Czeszak, Xavier; Lemoine, Jérôme; Roudbaraki, Morad; Cottet, J; Hondermarck, Hubert; Dugimont, Thierry; Curgy, Jean-Jacques

doi:10.1038/sj.onc.1205233

Cited by 47 publications

(31 citation statements)

References 49 publications

(46 reference statements)

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“…4). The spot distribution observed here is consistent and very similar to what was described for the MDA-MB-231 cells (Lottin et al, 2002). Nearly 800 spots were obtained in the range of molecular weight 15-250 kDa and pI 4-7.…”

Section: Proteome Changes In P75supporting

confidence: 73%

Proteome changes induced by overexpression of the p75 neurotrophin receptor (p75NTR) in breast cancer cells

Wilmet

Tastet²,

Desruelles³

et al. 2011

Int. J. Dev. Biol.

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In breast cancer cells, the neurotrophin receptor p75NTR acts as a prosurvival factor able to stimulate resistance to apoptosis, but its mechanism of action remains incompletely defined. In this study, we investigated the global proteome modification induced by p75 NTR overexpression in breast cancer cells treated by the pro-apoptotic agent tumor necrosis factor (TNF)-related-apoptosis-inducing-ligand (TRAIL). p75 NTR was stably overexpressed in the MCF-7 breast cancer cells and the impact of a treatment by TRAIL was investigated in wild type vs. p75 NTR overexpressing cells. Proteins were separated in two-dimensional electrophoresis, and regulated spots were detected by computer assisted analysis before identification by MALDI-TOF/TOF mass spectrometry. In the absence of TRAIL treatment, p75 NTR did not induce any change in the proteome of breast cancer cells. In contrast, after treatment with TRAIL, fragments of cytokeratin-8, -18 and -19, as well as full length cytokeratin-18, were up-regulated by p75 NTR overexpression. Of note, spectrin alpha-chain and the ribosomal protein RPLP0 were induced by TRAIL, independently of p75 NTR level. Interestingly, the well known stress-induced protein HSP-27 was less abundant when p75 NTR was overexpressed, indicating that p75 NTR overexpression reduced TRAIL induced cell stress. These data indicate that overexpression of p75 NTR induces proteome modifications in breast cancer cells and provide information on how this receptor contributes in tumor cell resistance to apoptosis.

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Section: Proteome Changes In P75supporting

confidence: 73%

Proteome changes induced by overexpression of the p75 neurotrophin receptor (p75NTR) in breast cancer cells

Wilmet

Tastet²,

Desruelles³

et al. 2011

Int. J. Dev. Biol.

Self Cite

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“…Based on the physical association of the H19 transcript with polysomes, the mechanism of H19 action is thought to be at the level of translational regulation (48). In addition, thioredoxin, a modulator of signal transduction and potentiator of tumorigenesis, was recently identified as translationally up-regulated by H19 (49). Further studies will undoubtedly elucidate other H19-regulated molecules and the role of H19 in both physiologic and pathologic settings.…”

Section: Discussionmentioning

confidence: 99%

The c-Myc Oncogene Directly Induces the H19 Noncoding RNA by Allele-Specific Binding to Potentiate Tumorigenesis

et al. 2006

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The product of the MYC oncogene is widely deregulated in cancer and functions as a regulator of gene transcription. Despite an extensive profile of regulated genes, the transcriptional targets of c-Myc essential for transformation remain unclear. In this study, we show that c-Myc significantly induces the expression of the H19 noncoding RNA in diverse cell types, including breast epithelial, glioblastoma, and fibroblast cells. c-Myc binds to evolutionarily conserved E-boxes near the imprinting control region to facilitate histone acetylation and transcriptional initiation of the H19 promoter. In addition, c-Myc down-regulates the expression of insulin-like growth factor 2 (IGF2), the reciprocally imprinted gene at the H19/ IGF2 locus. We show that c-Myc regulates these two genes independently and does not affect H19 imprinting. Indeed, allele-specific chromatin immunoprecipitation and expression analyses indicate that c-Myc binds and drives the expression of only the maternal H19 allele. The role of H19 in transformation is addressed using a knockdown approach and shows that down-regulation of H19 significantly decreases breast and lung cancer cell clonogenicity and anchorage-independent growth. In addition, c-Myc and H19 expression shows strong association in primary breast and lung carcinomas. This work indicates that c-Myc induction of the H19 gene product holds an important role in transformation. (Cancer Res 2006; 66(10): 5330-7)

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“…It has been reported that H19 RNA was involved in the repression of the IGF-2 oncogene by affecting its transcription (11) or its translation (12). Recently, we brought evidence that the H19 gene post-transcriptionally up-regulates the thioredoxin level, a key protein of the cellular redox metabolism (13).…”

mentioning

confidence: 90%

H19 mRNA-like Noncoding RNA Promotes Breast Cancer Cell Proliferation through Positive Control by E2F1

Berteaux

Lottin

Monté³

et al. 2005

Journal of Biological Chemistry

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331

267

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The imprinted H19 gene has riboregulatory functions. We show here that H19 transcription is up-regulated during the S-phase of growth-stimulated cells and that the H19 promoter is activated by E2F1 in breast cancer cells. H19 repression by pRb and E2F6 confirms the E2F1-dependent control of the H19 promoter. Consistently, we demonstrate by chromatin immunoprecipitation assays that endogenous E2F1 is recruited to the H19 promoter in vivo. The functionality of E2F promoter sites was further confirmed by gel shift and mutagenesis experiments, revealing that these sites are required for binding and promoter response to E2F1 exogenous expression and serum stimulation. Furthermore, we show that H19 overexpression confers a growth advantage on breast cancer cells released from growth arrest as well as in asynchronously growing cells. The H19 knockdown by small interfering RNA duplexes impedes S-phase entry in both wild-type and stably H19-transfected cells. Based on these findings, we conclude that the H19 RNA is actively linked to E2F1 to promote cell cycle progression of breast cancer cells. This clearly supports the H19 oncogenic function in breast tumor genesis.

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Thioredoxin post-transcriptional regulation by H19 provides a new function to mRNA-like non-coding RNA

Cited by 47 publications

References 49 publications

Proteome changes induced by overexpression of the p75 neurotrophin receptor (p75NTR) in breast cancer cells

Proteome changes induced by overexpression of the p75 neurotrophin receptor (p75NTR) in breast cancer cells

The c-Myc Oncogene Directly Induces the H19 Noncoding RNA by Allele-Specific Binding to Potentiate Tumorigenesis

H19 mRNA-like Noncoding RNA Promotes Breast Cancer Cell Proliferation through Positive Control by E2F1

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