p53 Ser15 phosphorylation and histone modifications contribute to IR-induced miR-34a transcription in mammary epithelial cells

Wang, Bo; Li, Dongping; Kovalchuk, Olga

doi:10.4161/cc.25135

Cited by 24 publications

(17 citation statements)

References 64 publications

(81 reference statements)

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“…Upon p38α activation, over thirty transcription factors, including p53, can be directly phosphorylated, resulting in transcriptional activation in most cases. Moreover, several studies have also shown that p53 can regulate the transcription of microRNAs (miRNAs) [16][17][18] . miRNAs are small, non-coding RNAs (approximately 21-23 nucleotides) that can regulate the stability of their target messenger RNAs (mRNAs) and/or down-regulate their translation 19 .…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: p38/p53/miR-200a-3p feedback loop promotes oxidative stress-mediated liver cell death

Xiao

Yan

et al. 2015

Cell Cycle

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Although our previous studies have provided evidence that oxidative stress has an essential role in total parenteral nutrition (TPN)-associated liver injury, the mechanisms involved are incompletely understood. Here, we show the existence of crosstalk between the miR-200 family of microRNAs and oxidative stress. The members of the miR-200 family are markedly enhanced in hepatic cells by hydrogen peroxide (H2O2) treatment. The upregulation of miR-200-3p in turn modulates the H2O2-mediated oxidative stress response by targeting p38α. The enhanced expression of miR-200-3p mimics p38α deficiency and promotes H2O2-induced cell death. Members of the miR-200 family that are known to inhibit the epithelial to mesenchymal transition (EMT) are induced by the tumor suppressor p53. Here, we show that p53 phosphorylation at Ser 33 contributes to H2O2-induced miR-200s transcription. In addition, we show that p38α can directly phosphorylate p53 at serine 33 upon H2O2 exposure. Thus, we suggest that in liver cells, the oxidative stress-induced, p38α-mediated phosphorylation of p53 at Ser33 is essential for the functional regulation of oxidative stress-induced miR-200 transcription by p53. Collectively, our data indicate that the p53-dependent expression of miR-200a-3p promotes cell death by inhibiting a p38/p53/miR-200 feedback loop.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: p38/p53/miR-200a-3p feedback loop promotes oxidative stress-mediated liver cell death

Xiao

Yan

et al. 2015

Cell Cycle

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“…Furthermore, IR-induced p53 phosphorylation at Ser15 and modifications of histones H3 and H4 have been proposed as mechanisms for enhanced miR-34a transcription in irradiated cells. 47 With rare exceptions, miR-34a is transactivated by p53 wild-type. In GBM cell lines harboring a p53 mutation within the DNA-binding domain, miR-34a expression is abrogated (AK, RA, publication in preparation).…”

Section: Discussionmentioning

confidence: 99%

microRNA-34a promotes DNA damage and mitotic catastrophe

et al. 2013

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“…In this pathway, it had been concluded previously that some anti‐correlated genes of p53‐pathway had a different expression in irradiated human peripheral blood lymphocytes (PBL) (Girardi et al, ). In mammary epithelial cells, IR‐induced miR‐34a was correlated with the p53 at Ser15, of which the phosphorylated levels were obviously increased by 96 h IR (Wang et al, ). Calcium signaling pathway was reported that it played a leading role in transferring signal (Catterall et al, ).…”

Section: Resultsmentioning

confidence: 99%

“…All above these results, it illustrated that target genes of differently expressed miRNA took part in an extensive range of biological effects, especially for the transcription, modification, cell proliferation, and repair. In this process, many pathways were regulated by miRNAs through binding to downstream targets, such as p53 signaling pathway, which was a regulated phosphorylated level pathway (the O of COG classification) induced by IR (Wang et al, ). Meaningfully, these results demonstrated that IR could trigger off the differentially expressed miRNAs through direct energy deposition or reactive free radicals generation, further damaging normal liver, which were closely related to certain biological function (Koturbash et al, ; Seyed Jalal, ).…”

Section: Resultsmentioning

confidence: 99%

MiRNA expression profile of ionizing radiation‐induced liver injury in mouse using deep sequencing

Chen

Hao³

et al. 2016

Cell Biology International

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In order to investigate the potential regulatory roles of microRNAs (miRNAs) in mouse response to ionizing radiation (IR), the small RNA libraries from liver tissues of mice with or without ionizing radiation (IR) were sequenced by high-throughput deep sequencing technology. A total of 270 miRNAs including 212 known and 58 potentially novel miRNAs were identified. Within these miRNAs, there were 48 miRNAs that were differentially expressed, including 27 known and 21 novel miRNAs. The results of quantitative RT-polymerase chain reaction (qRT-PCR) were in consistent with the sequencing analysis. Target gene prediction, function annotation, and pathway of the identified miRNAs were analyzed using RNAhybrid, miRanda software and Swiss-Prot, Gene Ontology (GO), Clusters of Orthologous Groups (COG), Kyoto Encyclopedia of Genes, and Genomes (KEGG) and non-redundant (NR) databases. These results should be useful to investigate the biological function of miRNAs under IR-induced liver injury.

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p53 Ser15 phosphorylation and histone modifications contribute to IR-induced miR-34a transcription in mammary epithelial cells

Cited by 24 publications

References 64 publications

RETRACTED ARTICLE: p38/p53/miR-200a-3p feedback loop promotes oxidative stress-mediated liver cell death

RETRACTED ARTICLE: p38/p53/miR-200a-3p feedback loop promotes oxidative stress-mediated liver cell death

microRNA-34a promotes DNA damage and mitotic catastrophe

MiRNA expression profile of ionizing radiation‐induced liver injury in mouse using deep sequencing

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