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Inactivation of Oncogenic cAMP-specific Phosphodiesterase 4D by miR-139-5p in Response to p53 Activation

ABSTRACT: Investigation of microRNA expression level changes in human colon cancer cell lines in response to p53 activation by Inauhzin (INZ), and identification of novel p53 target microRNAs. HCT116 p53+/+ and HCT116 p53-/- cells were treated with DMSO or 4Î¼M INZ and harvested at 18 hours post treatment. Cells were then homogenized in TriZol reagents. Duplicates were included for each sample. Total RNA was extracted by following the manufacturerâs standard instructions (Invitrogen).

ORGANISM(S): Homo sapiens

SUBMITTER: HUA LU

PROVIDER: E-GEOD-79099 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Inactivation of Oncogenic cAMP-specific Phosphodiesterase 4D by miR-139-5p in Response to p53 Activation

Project description:Investigation of microRNA expression level changes in human colon cancer cell lines in response to p53 activation by Inauhzin (INZ), and identification of novel p53 target microRNAs.

2016-07-20 | GSE79099 | GEO

shRNA profiling of human hepatocyte HepG2 cells knocked down for HNF4 to investigate its role in inflammatory response

Project description:To obtain a genomic view of hepatocyte nuclear factor-4Î± (HNF-4Î±) in the regulation of the inflammatory response, microarray analysis was used to probe the expression profile of an inflammatory response induced by cytokines in a model of knock-down HNF-4Î± HepG2 cells. The results indicate an extensive role for HNF-4Î± plays in the regulation of a large number of the liver-specific genes. Majority of genes (71%) affected by cytokine treatment are also affected by HNF-4Î± knock-down. This significant overlap suggests that HNF-4Î± may play a role in regulating the cytokine-induced inflammatory response. Experiment Overall Design: The different treated HepG2 cells were grouped into 4 groups (four replicates in each group): Group1, Control; Group2, HNF-4Î± shRNA treated cells; Group3, cytokine treated group; Group4, HNF-4Î± shRNA and cytokine treatments. RNA extraction and hybridization on Affymetrix microarrays were processed. The expression profiles between different groups were analyzed and compared. In order to explore the function of HNF-4Î± in the inflammatory response, a set of 170 genes annotated as inflammatory response was obtained from GO (geneotology.org), the enrichments of these inflammatory genes were analyzed in different treated groups.

2009-05-16 | E-GEOD-15991 | biostudies-arrayexpress

Inactivation of oncogenic cAMP-specific phosphodiesterase 4D by miR-139-5p in response to p53 activation.

Project description:Increasing evidence highlights the important roles of microRNAs in mediating p53's tumor suppression functions. Here, we report miR-139-5p as another new p53 microRNA target. p53 induced the transcription of miR-139-5p, which in turn suppressed the protein levels of phosphodiesterase 4D (PDE4D), an oncogenic protein involved in multiple tumor promoting processes. Knockdown of p53 reversed these effects. Also, overexpression of miR-139-5p decreased PDE4D levels and increased cellular cAMP levels, leading to BIM-mediated cell growth arrest. Furthermore, our analysis of human colorectal tumor specimens revealed significant inverse correlation between the expression of miR-139-5p and that of PDE4D. Finally, overexpression of miR-139-5p suppressed the growth of xenograft tumors, accompanied by decrease in PDE4D and increase in BIM. These results demonstrate that p53 inactivates oncogenic PDE4D by inducing the expression of miR-139-5p.

| S-EPMC4959878 | biostudies-literature

MiR-139-5p has an antidepressant-like effect by targeting phosphodiesterase 4D to activate the cAMP/PKA/CREB signaling pathway.

Project description:BackgroundPhosphodiesterase 4D (PDE4D) inhibitor is commonly used to treat depression, but side effects seriously decrease its efficacy. PDE4D was a downstream target mRNA of miR-139-5p. Therefore, we examined the effects of hippocampal miR-139-5p gain- and loss-of-function on depression-like behaviors, the expression level of PDE4D, and hippocampus neurogenesis.MethodsBioinformatic analyses were carried out to to screen differential genes. Quantitative real-time polymerase chain reaction (qRT-PCR) and luciferase reporter assay were used to confirm the relationship between miR-139-5p and PDE4D. MiR-139-5p mimics, miR-139-5p inhibitor, or miR-NC were used to explore the function of miR-139-5p in HT-22 cells. We further explored the role of miR-139-5p in vivo using AAV-injection. Elisa, western blotting, and fluorescence in situ hybridization (FISH) were used to detect the expression of miR-139-5p and PDE4D in CRC tissues.ResultsHere, we showed that PDE4D messenger RNA (mRNA) was a direct target of microRNA (miR)-139-5p, which was downregulated in a chronic ultra-mild stress (CUMS)-induced depression mouse model. Moreover, in experiments in vitro, miR-139-5p mimic repressed PDE4D expression in HT-22 cells, but promoted phosphorylated cyclic-AMP response element-binding protein (p-CREB) and brain-derived neurotrophic factor (BDNF) expression. Interestingly, adeno-associated virus (AAV)-miR-139-5p downregulated susceptibility to stress-induced depression-like behaviors in mice. AAV-miR-139-5p suppressed PDE4D in mouse hippocampal cells, increasing expression level of cyclic adenosine monophosphate (cAMP), p-CREB, and BDNF, and stimulating mouse hippocampal neurogenesis.ConclusionsOur findings suggested that miR-139-5p acted like an antidepressant by targeting PDE4D, thereby regulating the cAMP/protein kinase A (PKA)/CREB/BDNF pathway to improve depression.

| S-EPMC8576692 | biostudies-literature

Mutant p53 cancers reprogram macrophages to tumor supporting macrophages via exosomal miR-1246

Project description:exosomes isolated from: HT29+control shRNA; HT29+p53 shRNA; HCT116 WT p53; HCT116 mutant p53; HCT116 null p53; media used as negative control

2018-02-09 | MSV000082047 | MassIVE

Cell Context Dependent p53 Genome-Wide Binding Patterns and Enrichment at Repeats

Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin. Identification of genomic p53 binding sites in HCT116 cells by ChIP-seq.

2014-11-21 | E-GEOD-58714 | biostudies-arrayexpress

Phosphodiesterase 4D inhibitors limit prostate cancer growth potential.

Project description:UnlabelledPhosphodiesterase 4D (PDE4D) has recently been implicated as a proliferation-promoting factor in prostate cancer and is overexpressed in human prostate carcinoma. However, the effects of PDE4D inhibition using pharmacologic inhibitors have not been examined in prostate cancer. These studies examined the effects of selective PDE4D inhibitors, NVP-ABE171 and cilomilast, as anti-prostate cancer therapies in both in vitro and in vivo models. The effects of PDE4D inhibitors on pathways that are critical in prostate cancer and/or downstream of cyclic AMP (cAMP) were examined. Both NVP-ABE171 and cilomilast decreased cell growth. In vitro, PDE4D inhibitors lead to decreased signaling of the sonic hedgehog (SHH), androgen receptor (AR), and MAPK pathways, but growth inhibition was best correlated to the SHH pathway. PDE4D inhibition also reduced proliferation of epithelial cells induced by paracrine signaling from cocultured stromal cells that had activated hedgehog signaling. In addition, PDE4D inhibitors decreased the weight of the prostate in wild-type mice. Prostate cancer xenografts grown in nude mice that were treated with cilomilast or NVP-ABE171 had decreased wet weight and increased apoptosis compared with vehicle-treated controls. These studies suggest the pharmacologic inhibition of PDE4D using small-molecule inhibitors is an effective option for prostate cancer therapy.ImplicationsPDE4D inhibitors decrease the growth of prostate cancer cells in vivo and in vitro, and PDE4D inhibition has therapeutic potential in prostate cancer.

| S-EPMC4312503 | biostudies-literature

Transcription profiling of rat primary hepatocyte in culture after low dose and short incubation time of cadmium in primary

Project description:The study was performed using primary rat hepatocyte in culture from 4 adult male Sprague-Dawley rats to investigate the changes in gene expression under low dose (4Î¼M) and short exposure (3hrs) of cadmium chloride. By comparing the gene expression profiles of control and cadmium-treated cells, the most dramatic and significant changes were for those genes associated with transcriptional regulation, antioxidant response and control of protein integrity. Changes in other genes involved in cellular physiological responses such as inflammation, growth and apoptosis were also observed. Results were further confirmed by quantitative real time polymerase chain reaction (qRT-PCR). Experiment Overall Design: Primary hepatocytes from four rats were isolated using the collagenase-hyaluronidase perfusion and digestion method. The cells of greater than 85% viability were used in this study. The cells were plated at 90% confluency on culture dishes coated with collagen and maintained in Waymouth's medium containing BSA for 4hrs prior to an overnight incubation with BSA free Waymouth's medium. Control samples and cadmium-treated samples from individual rats were hybridized to RAE 230A arrays (n=4 and 8 microarrays); data were generated and analyzed.

2009-03-07 | E-GEOD-8013 | biostudies-arrayexpress

Crotonylomics sequencing of human colon cancer cell lines

Project description:P53 mutation is closely associated with the occurrence and progression of colon cancer. In this project, we did crotonylomics sequencing by using human colon cancer homologous cell line pair-HCT116+/+(with wild type p53) and HCT116-/- (with null p53). Crotonylomics sequencing results showed that p53 deficiency regulated crotonylation of non-histone proteins.

2024-05-22 | PXD047258 | Pride

Genome-wide miRNA-expression analysis after p53 activation in colorectal cancer cells

Project description:In order to comprehensively identify miRNA-expression changes after p53-activation a miRNA-Seq analysis was conducted after activation of a conditional p53 allele in SW480 cells. SW480/pRTR-p53-VSV cells were subjected to miRNA-Seq analysis after 16 hours doxycycline-treatment. Kompetenzzentrum für fluoreszente Bioanalytik, Regensburg, Germany

2015-07-21 | E-GEOD-67181 | biostudies-arrayexpress

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