Interaction between p53 and estradiol pathways in transcriptional responses to chemotherapeutics

Lion, Mattia; Bisio, Alessandra; Tebaldi, Toma; Sanctis, Veronica De; Menéndez, Daniel; Resnick, Michael A.; Ciribilli, Yari; Inga, Alberto

doi:10.4161/cc.24309

Cited by 35 publications

(45 citation statements)

References 71 publications

(93 reference statements)

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“…This correlated with an accumulation of p53 protein and induction of apoptosis in the embryonic stem cells in hypoxia (Supplemental Figure 4E). These data together demondescribed as a p53 target gene with 2 p53 REs in intron 9 (36). We carried out ChIP analysis using both these REs and found that one of them was moderately enriched for p53 binding in hypoxia (Supplemental Figure 4A).…”

Section: Resultsmentioning

confidence: 99%

Hypoxia-induced p53 modulates both apoptosis and radiosensitivity via AKT

Leszczynska¹,

Foskolou²,

Abraham³

et al. 2015

J. Clin. Invest.

122

114

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Section: Resultsmentioning

confidence: 99%

Hypoxia-induced p53 modulates both apoptosis and radiosensitivity via AKT

Leszczynska¹,

Foskolou²,

Abraham³

et al. 2015

J. Clin. Invest.

122

114

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“…1 Although the role of p53 is generally considered to be at the level of transactivation via binding to target sequences, there are several other ways by which it can determine its cellular responses including, for example, interaction with other transcription factors. 2 Post-transcriptional and translational controls provide fine tuning of transcriptional outcomes in eukaryotic somatic cells. 3 More than 90% of all coding transcripts appear to be subject to this regulation, especially at translation initiation, 4 considered as the rate-limiting step of the whole process.…”

mentioning

confidence: 99%

“…59 Rapamycin (Sigma-Aldrich)-Torin1 (Tocris Bioscience, Bristol, UK). Proteins were extracted using RIPA buffer as previously described, 2 supplemented with protease inhibitors and phosphatase inhibitor cocktail2 (Sigma-Aldrich) and quantified using the BCA assay (Thermo Scientific, Pierce, Milan, Italy). The relative molecular mass of the immunoreactive bands was determined using PageRuler Plus Prestained Protein Ladder (Fermentas).…”

mentioning

confidence: 99%

p53-directed translational control can shape and expand the universe of p53 target genes

et al. 2014

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The increasing number of genome-wide transcriptome analyses focusing on p53-induced cellular responses in many cellular contexts keeps adding to the already numerous p53-regulated transcriptional networks. To investigate post-transcriptional controls as an additional dimension of p53-directed gene expression responses, we performed a translatome analysis through polysomal profiling on MCF7 cells upon 16 hours of doxorubicin or nutlin-3a treatment. The comparison between the transcriptome and the translatome revealed a considerable level of uncoupling, characterized by genes whose transcription variations did not correlate with translation variations. Interestingly, uncoupled genes were associated with apoptosis, DNA and RNA metabolism and cell cycle functions, suggesting that post-transcriptional control can modulate classical p53-regulated responses. Furthermore, even for well-established p53 targets that were differentially expressed both at the transcriptional and translational levels, quantitative differences between the transcriptome, subpolysomal and polysomal RNAs were evident. As we searched mechanisms underlying gene expression uncoupling, we identified the p53-dependent modulation of six RNA-binding proteins, where hnRNPD (AUF1) and CPEB4 are direct p53 transcriptional targets, whereas SRSF1, DDX17, YBX1 and TARDBP are indirect targets (genes modulated preferentially in the subpolysomal or polysomal mRNA level) modulated at the translational level in a p53-dependent manner. In particular, YBX1 translation appeared to be reduced by p53 via two different mechanisms, one related to mTOR inhibition and the other to miR-34a expression. Overall, we established p53 as a master regulator of translational control and identified new p53-regulated genes affecting translation that can contribute to p53-dependent cellular responses.

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“…Acting as an inhibitor of the PI3K pathway, INPP5D is considered as a tumor suppressor in acute myeloid leukemia, Hodgkin's lymphoma, and acute lymphoblastic leukemia (Luo et al 2004;Metzner et al 2009;Tiacci et al 2012). Besides, INPP5D has been found as the target of the cellular tumor antigen p53 in human breast cancer adenocarcinoma MCF7 cells and testicular germ cell tumor-derived human embryonal carcinoma cells (Kerley-Hamilton et al 2005;Lion et al 2013). Although the role INPP5D plays in prostate tumor cells has not been established, it is possible that INPP5D contributes to prostate cancer progression through the PI3K or p53 pathway.…”

Section: Discussionmentioning

confidence: 99%

Screening for Novel Germline Rare Mutations Associated with Aggressive Prostate Cancer

Chen¹

2014

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Interaction between p53 and estradiol pathways in transcriptional responses to chemotherapeutics

Cited by 35 publications

References 71 publications

Hypoxia-induced p53 modulates both apoptosis and radiosensitivity via AKT

Hypoxia-induced p53 modulates both apoptosis and radiosensitivity via AKT

p53-directed translational control can shape and expand the universe of p53 target genes

Screening for Novel Germline Rare Mutations Associated with Aggressive Prostate Cancer

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