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Phosphodiesterase 10A (PDE10A) as a novel target to suppress β-catenin and RAS signaling in ovarian cancer

ABSTRACT: Phosphodiesterase 10A (PDE10A) as a novel target to suppress β-catenin and RAS signaling in ovarian cancer

PROVIDER: PRJNA690803 | ENA |

REPOSITORIES: ENA

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Phosphodiesterase 10A (PDE10A) as a novel target to suppress β-catenin and RAS signaling in ovarian cancer

Project description:The goal of this study was to investigate molecular pathways associated with PDE10A in ovarian cancer. We used CRISPR/Cas9 to knockout PDE10A in SKOV3 cells. We used the Illumina NextSeq500 to generate between 30-35 million paired end 75bp sequencing reads per sample for transcript level abundance.

2022-01-10 | GSE164474 | GEO

Transcription profiling of human colorectal adenocarcinoma samples transfected with a miR-10a repressor to identify candidate target genes of miR-10a

Project description:MiR-10a inhibits colon cancer invasion and metastasis. To search the candidate target genes of miR-10a, SW480 cells were transfected with miR-10a blockage to suppress miR-10a activity and the differentially expressed genes were detected by cDNA microarray analysis. Some of the up-regulated genes may be candidate target genes of miR-10a.

2009-02-20 | E-MEXP-2061 | biostudies-arrayexpress

Phosphodiesterase 10A inactivation protects against doxorubicin-induced cardiotoxicity and concomitantly inhibits tumor growth

Project description:Phosphodiesterase 10A (PDE10A), by degrading cAMP/cGMP, play critical roles in cardiovascular biology/disease. Cardiotoxicity is a clinical complication of chemotherapy. We aim to determine the role of PDE10A in cancer growth and cardiotoxicity induced by doxorubicin (DOX), a chemotherapy drug. We found that PDE10A deficiency/inhibition alleviated DOX-induced cardiotoxicity in C57Bl/6J mice, including myocardial atrophy, apoptosis, and dysfunction. RNAseq study revealed several PDE10A-regulated signaling associated with DOX-induced cardiotoxicity. In cancer cells, PDE10A inhibition increased the death, decreased the proliferation, and potentiated the effect of DOX in various cancer-cell lines. Importantly, in nude mice with implanted ovarian cancer xenografts, PDE10A inhibition attenuated tumor growth while protected against DOX-induced cardiotoxicity. In isolated cardiomyocytes (CMs), PDE10A contributed to DOX-induced CM death via promoting mitochondrial dysfunction, and to CM atrophy via potentiating foxo3 signaling. Collectively, our study elucidates a novel role for PDE10A in cardiotoxicity and cancer growth in vitro and in vivo, and suggest that PDE10A inhibition may represent a novel strategy in cancer therapy.

2023-06-22 | GSE224157 | GEO

Gene expression profiles MCF-10A cells overexpressing MBD2

2013-06-17 | GSE47873 | GEO

Gene expression profiles MCF-10A cells overexpressing MBD2

2013-06-17 | E-GEOD-47873 | biostudies-arrayexpress

Phosphodiesterase 10A is overexpressed in lung tumor cells and inhibitors selectively suppress growth by blocking ?-catenin and MAPK signaling.

Project description: Not available

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The Wnt/β-catenin and RAS-ERK Pathways were Activated in Tissues of Chemotherapy-Resistant Gastric Cancer PDX Tumor

Project description:Chemotherapy resistance and disease recurrence remains major causes of gastric cancer patient mortality. We describe possible relationship between Wnt/b-catenin and RAS/ERK pathways in GC patients and acquired-resistant GC PDX tumors against FOLFOX, 5-fluorouracil-based chemotherapy. RNA sequencing analysis also demonstrates that Wnt/b-catenin pathway is an actionable target pathway for overcoming the chemotherapy resistance. These provide that an approach targeting both Wnt/b-catenin and RAS/ERK pathways could be novel therapeutic strategy in GC resistant to standard chemotherapy.

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Methylation profiles of MCF-10A cells infected with MBD2 lentivirus

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Phosphodiesterase 3A deficient in breast cancer cell

Project description:Analysis of MDA-MB-231 breast tumor cell from knocking-down phosphodiesterase 3A (PDE3A), a cyclic nucleotide phosphodiesterase. Results provide insight into the role of PDE3A in breast tumor progression and metastasis.

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Methylation profiles of MCF-10A cells infected with MBD2 lentivirus

Project description:Methylated DNA binding protein 2 (MBD2) has been shown to bind specific methylated promoters and suppress transcription. Here we systematically investigate MBD2 suppression by overexpressing MBD2 in MCF-10A cells and generating genome-wide promoter methylation profiles in order to identify methylation changes likely to affect gene expression levels. MCF-10A cells were infected with MBD2 lentivirus in order to increase MBD2 expression. DNA was extracted from both infected and non-infected cells and enriched for methylated DNA through the method of methylated DNA immunoprecipitation (MeDIP). Enriched and total DNA was hybridized in different channels to 244K custom microarrays (Agilent Technologies) that contained probes covering at 100bp-spacing all transcription start sites from -800bp to 200bp (human, Ensembl v44) and all microRNAs in miRBase from 250bp before to 250bp after the microRNA. Three technical replicates were hybridized for infected and non-infected cells.

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