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Histone Deacetylase Inhibitor prevents cell growth in Burkitt's lymphoma by regulating PI3K/Akt pathways and leading to up regulation of micro RNA-143, -145 and -101

ABSTRACT: In this study we analyzed gene expression profiles in a well-characterized BL cell line upon treatment with HDACi combined with chemotherapy. The impact on gene expression regulation was broader when HDACi was combined with chemotherapy, than when either therapy was used alone. As expected, treatment interfered in the regulation of cell cycle progression and enhanced cell death. Noteworthy was the effect on members of p53 signaling pathway. The down regulation of PI3KCA and up regulation of p16 were observed at the gene and protein levels, while the inhibition of Akt phosphorylation and the down regulation of c-Myc were confirmed through the analysis of protein levels. As a complementary approach we investigated if HDACi combined with chemotherapy treatment would enhance mir-101, mir-143 and mir-145 levels in BL cell line. This hypothesis was confirmed and we also observed that levels of mir-101, mir-143 and mir-145 were extremely down regulated in BL patients' samples. In this study we demonstrate mechanisms involved in cell cycle arrest upon cell treatment using a combination of HDACi and chemotherapy. We highlight the fact that effective combinations of HDACis with other cytotoxic drugs could improve BL therapy in the future.

ORGANISM(S): Homo sapiens

PROVIDER: GSE48399 | GEO | 2014/06/20

SECONDARY ACCESSION(S): PRJNA209946

REPOSITORIES: GEO

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Histone Deacetylase Inhibitor prevents cell growth in Burkitt's lymphoma by regulating PI3K/Akt pathways and leading to up regulation of micro RNA-143, -145 and -101

Project description:In this study we analyzed gene expression profiles in a well-characterized BL cell line upon treatment with HDACi combined with chemotherapy. The impact on gene expression regulation was broader when HDACi was combined with chemotherapy, than when either therapy was used alone. As expected, treatment interfered in the regulation of cell cycle progression and enhanced cell death. Noteworthy was the effect on members of p53 signaling pathway. The down regulation of PI3KCA and up regulation of p16 were observed at the gene and protein levels, while the inhibition of Akt phosphorylation and the down regulation of c-Myc were confirmed through the analysis of protein levels. As a complementary approach we investigated if HDACi combined with chemotherapy treatment would enhance mir-101, mir-143 and mir-145 levels in BL cell line. This hypothesis was confirmed and we also observed that levels of mir-101, mir-143 and mir-145 were extremely down regulated in BL patients' samples. In this study we demonstrate mechanisms involved in cell cycle arrest upon cell treatment using a combination of HDACi and chemotherapy. We highlight the fact that effective combinations of HDACis with other cytotoxic drugs could improve BL therapy in the future. DNA microarrays were used to access global gene expression modulation upon treatment of Raji BL cell line with VP-16 or NaB and a combination of NaB and VP-16 for 24 hours. Total RNA was extracted using TrizolM-BM-.. Gene expression of treated cells was compared with controls consisting of untreated cells. Microarray analysis was performed using Agilent Whole Human Genome Microarray 4M-CM-^W44K arrays and labeled using the One Color Quick Amp Labeling Kit (Agilent Technologies). Two biological replicates were included for each experimental condition.

2014-06-20 | E-GEOD-48399 | biostudies-arrayexpress

The mir-143-145 cluster plays a pro-tumorigenic role in lung adenocarcinoma by promoting neoangiogenesis

Project description:A growing body of literature has proposed cell-autonomous tumor suppressor functions for the mir-143~145 cluster in a variety of human cancers, including lung adenocarcinoma, and has reported therapeutic benefits of delivering mir-143 and mir- 145 to tumors. In contrast to these studies, we found that depletion or forced expression of mir-143 and mir-145 in an autochthonous mouse model of lung adenocarcinoma did not affect tumor development. Surprisingly, we observed that loss of mir-143~145 from the tumor microenvironment significantly reduced tumor burden, indicating a non-cell- autonomous role for these miRNAs in promoting tumorigenesis. By examining the expression patterns of different cell populations isolated in vivo from tumor-bearing lungs using an integrated computational approach, we identified a role for mir-145 in stimulating the proliferation of endothelial cells by downregulating an inhibitory kinase, Camk1d, which prevents mitotic entry. As a consequence, tumors in mir-143~145- deficient animals exhibited diminished hallmarks of neo-angiogenesis, increased apoptosis and their expansion appeared limited by the tumor’s ability to co-opt the alveolar vasculature. These findings show that expression of the mir-143~145 cluster in the tumor stroma promotes rather than suppresses tumorigenesis and cautions against the use of these miRNAs as agents in cancer therapeutics.

2016-05-21 | GSE71877 | GEO

Analysis of miR-143/145 wild-type and null mouse intestinal myofibroblasts before and after LPS stimulation

Project description:In a series of mouse genetic studies, we concluded that miR-143/145 expression in intestinal subepithelial myofibroblasts (ISEMFs) promotes epithelial regeneration after DSS-mediated injury in the colon. This experiment aims to identify miR-143/145 target genes that are involved in this function. We generated primary ISEMFs from wildtype and miR-143/145 null mouse colons and analyzed their gene expression profile. We further subjected ISEMFs to LPS treatment, in order to measure gene expression changes that are only revealed after inflammatory stress.

2014-05-22 | GSE55651 | GEO

Mouse ureter: wild type vs miR-143/145 knock out

Project description:mRNA profiling of mouse ureters comparing wild-type ureter vs. ureters from mice having whole body deletion of miR-143 and miR-145 which results in abnormal ureter peristalsis and hydronephrosis We used microarrays to detail the global program of gene expression in wild-type and miR-143/145-deficient ureters which revealed dysregulation of genes linked to smooth muscle morphology and function. Two condition experiment: wild type vs miR-143/145 KO; biological replicates: individual mice - 2 wild type, 2 mutant. One replicate per array.

2014-10-08 | E-GEOD-58274 | biostudies-arrayexpress

Analysis of miR-143/145 wild-type and null mouse intestinal myofibroblasts before and after LPS stimulation

2014-05-22 | E-GEOD-55651 | biostudies-arrayexpress

Expression data from primary hepatocytes isolated from miR-143DOX mice

2011-04-08 | GSE26460 | GEO

Mouse ureter: wild type vs miR-143/145 knock out

2014-10-08 | GSE58274 | GEO

Expression data from primary hepatocytes isolated from miR-143DOX mice

Project description:The contribution of altered posttranscriptional gene silencing (PTGS) to the development of insulin resistance and type 2 diabetes mellitus so far remains elusive. We have described that expression of microRNAs (miR)-143 and -145 is dysregulated in genetic and dietary mouse models of obesity. Induced transgenic overexpression of miR-143, but not miR-145, causes insulin resistance and impaired insulin-stimulated AKT activation. We used microarrays to analyze the underlying molecular mechanisms of miR-143-mediated development of insulin resistance. miR-143DOX mice (n=3) and wildtype littermate controls (n=3) were treated with doxycycline via the drinking water to induce miR-143 overexpression in the transgenic animals. Primary hepatocytes were isolated for RNA extraction and hybridization on Affymetrix microarrays.

2011-04-08 | E-GEOD-26460 | biostudies-arrayexpress

RNA-Seq analysis of human M238P melanoma cells transduced with a lentivirus expressing the miR-143/145 cluster or a control lentivirus

Project description:To assess the transcriptomic response associated with upregulation of the miR-143/-145 cluster, BRAFV600E mutant human melanoma cells M238P cells were transduced for stable expression of miR-143/145 cluster or with a control vector. Forty-eight hours after transduction, cells were treated with 1 μg/mL of puromycin for one week. RNA samples were then harvested. Two independent experiments were carried out.

2021-12-29 | GSE171881 | GEO

rs41291957 alters secondary RNA structure of the human pri-miR-143/145

Project description:Purpose: To evaluate whether the single nucleotide polimorphsim rs41291957, located in the pri-miR-143/145, influences the primary RNA secondary structure. Methods: In vitro transcription and folding for the pri-miR-143/145 carrying the WT allele (G) or the mutated one (A) was carried out. The RNAs were then subjected to RNAseI treatement for 30 minutes and RNA seq performed on the digested nucleic acids. Results: Using an optimized data analysis workflow for small RNAs, we mapped the sequence reads on the human pri-miR-143/145 carrying the G- or A-allele. We observed an increase of small reads (<60bps) for the A-allele and a different profile of read enrichement between the digested G- and A-allele RNA, indicating the difference in secondary structure.

2021-07-15 | GSE180017 | GEO

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