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Gene expression changes resulting from attenuation of Dicer activity

ABSTRACT: Despite smaller primary tumor burdens, Pten-/-Dicer-/+ mice develop seminal vesicle obstruction at high penetrance by 32 weeks, which is in sharp contrast to that observed in Pten-/- mice. This phenomenon implies that tumors in Pten-/-Dicer-/+ mice are more locally invasive. To corroborate this invasive phenotype, we examined global changes in gene expression using Agilent 44k whole genome expression microarrays. A total of 544 genes were statistically significantly altered by at least 1.4 fold in either Pten-/-Dicer-/+ or Pten-/-Dicer-/- mice, or both mice, as compared with Pten-/- mice. Approximately 22% genes were altered in the same trend in both Pten-/-Dicer-/+ and Pten-/-Dicer-/- mice, while 70% genes were only significantly affected in Pten-/-Dicer-/- mice. Very few genes were differentially regulated between Pten-/-Dicer-/+ and Pten-/-Dicer-/- mice or were only altered in Pten-/-Dicer-/+ mice. Data analysis identified that a list of genes associated with epithelial-mesenchymal transition, cell adhesion, migration, and extracellular matrix deposition are statistically significantly altered in favor of tumor metastasis in the Pten-/-Dicer-/+ mice. QRT-PCR confirmed the changes in expression of some genes including growth factors (Tgfb1 and Ctgf), transcription factors (Snail, Twist2, and Foxc1), protease (MMPs etc.), and extracellular matrix components (Collagens). This finding corroborates the phenotypic invasiveness of the tumors in Pten-/-Dicer-/+ mice at a molecular level.

ORGANISM(S): Mus musculus

PROVIDER: GSE42820 | GEO | 2013/07/17

SECONDARY ACCESSION(S): PRJNA183502

REPOSITORIES: GEO

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Gene expression changes resulting from attenuation of Dicer activity

Project description:Despite smaller primary tumor burdens, Pten-/-Dicer-/+ mice develop seminal vesicle obstruction at high penetrance by 32 weeks, which is in sharp contrast to that observed in Pten-/- mice. This phenomenon implies that tumors in Pten-/-Dicer-/+ mice are more locally invasive. To corroborate this invasive phenotype, we examined global changes in gene expression using Agilent 44k whole genome expression microarrays. A total of 544 genes were statistically significantly altered by at least 1.4 fold in either Pten-/-Dicer-/+ or Pten-/-Dicer-/- mice, or both mice, as compared with Pten-/- mice. Approximately 22% genes were altered in the same trend in both Pten-/-Dicer-/+ and Pten-/-Dicer-/- mice, while 70% genes were only significantly affected in Pten-/-Dicer-/- mice. Very few genes were differentially regulated between Pten-/-Dicer-/+ and Pten-/-Dicer-/- mice or were only altered in Pten-/-Dicer-/+ mice. Data analysis identified that a list of genes associated with epithelial-mesenchymal transition, cell adhesion, migration, and extracellular matrix deposition are statistically significantly altered in favor of tumor metastasis in the Pten-/-Dicer-/+ mice. QRT-PCR confirmed the changes in expression of some genes including growth factors (Tgfb1 and Ctgf), transcription factors (Snail, Twist2, and Foxc1), protease (MMPs etc.), and extracellular matrix components (Collagens). This finding corroborates the phenotypic invasiveness of the tumors in Pten-/-Dicer-/+ mice at a molecular level. Cancerous urogenital tissues from Pten-/- (Dicer WT), Pten-/-Dicer-/+ (Dicer HET), and Pten-/-Dicer-/- (Dicer KO) mice were profiled for gene expression, using Agilent microarrays. multiple group comparison

2013-07-17 | E-GEOD-42820 | biostudies-arrayexpress

Transcriptome analysis of control and BRG1-depleted 22RV-1 cells with or without PTEN ablation

Project description:We conduct transcriptome comparison of control and BRG1-depleted 22RV-1 cells with or without PTEN ablation to gain genomic insights on the biological processes that BRG1 is involved in depend on PTEN deletion. Through unsupervised cluster analysis of differentially expressed genes (DEGs), we found the expressions of 5489 genes were significantly altered in PTEN/BRG1 double knockdown cells, whereas they remained consistent or opposite pattern in control, BRG1-KD and PTEN-KD cells. Differential principal component analysis (PCA) suggested ablation of BRG1 in PTEN-depleted cells forced the cells undergoing a distinct transcriptome as compared to the others. In keeping with these findings, KEGG-DEGs relationship network indicated BRG1 loss in PTEN-deficient cells significantly altered the process related to “Prostate cancer”, “Cell cycle”, “Cell motility” and etc.

2019-01-14 | GSE115616 | GEO

Gene expression analysis of ovarian tumors from mice with knockout of DICER and PTEN

Project description:The cell of origin of serious ovarian cancer is unknown. To create a mouse model for this lethal cancer and identify early cancer biomarkers, we conditionally deleted both Dicer (essential for microRNA biosynthesis) and Pten (a negative regulator of the PI3K pathway) in the female reproductive tract. Beginning at ~3-5 months, these Dicer/Pten mutant mice develop high-grade serious carcinomas that initiate in the stroma of the fallopian tube through a mesenchymal-to-epithelial transition (MET), subsequently envelop the ovary, and then metastasize throughout the peritoneum, resulting in ascites and 100% lethality by 13 months. The fallopian tube cancers demonstrate upregulation of genes encoding known and novel secreted proteins that are potential biomarkers. This study uncovers a new paradigm for the initiation of high-grade serous ovarian cancer. RNA was isolated from the fallopian tube cancers of independent DKO mice and normal fallopian tubes of control mice and subjected to mRNA expression analysis using an Illumina platform (MouseWG-6 v2 Expression BeadChip).

2012-02-16 | E-GEOD-28720 | biostudies-arrayexpress

Migration and invasion of 5 glioblastoma cell lines

Project description:Glioblastoma cells are characterized by a highly invasive behavior whose mechanisms are not yet understood. Using the wound healing and Boyden chamber assays we compared in the present study the migration and invasion abilities of 5 glioblastoma cell lines (DK-MG, GaMG, U87-MG, U373-MG, SNB19) differing in p53 and PTEN status. We also analyzed by Western blotting the expression of PTEN, p53, mTOR and several other marker proteins involved in cell adhesion, migration and invasion. Among 5 cell lines, GaMG cells exhibited the fastest rate of wound closure, whereas U87-MG cells showed the most rapid chemotactic migration in the Boyden chamber assay. In DK-MG and GaMG cells, F-actin mainly occurred in the numerous stress fibers spanning the cytoplasm, whereas U87-MG, U373-MG and SNB19 cells preferentially expressed F-actin in filopodia and lamellipodia. Moreover, the two glioblastoma lines mutated in both p53 and PTEN genes (U373-MG and SNB19) were found to exhibit the fastest invasion rates through the Matrigel matrix. Here, we performed a gene expression profiling of the five glioblastoma cell lines to examine the molecular framework of differences in invasive behavior to find possible targets for chemo- and radiation therapy.

2014-09-05 | E-GEOD-53124 | biostudies-arrayexpress

Gene expression profiles of serous ovarian cancer in human and mouse

Project description:This SuperSeries is composed of the following subset Series: GSE28720: Gene expression analysis of ovarian tumors from mice with knockout of DICER and PTEN GSE28721: Gene expression analysis of human serious ovarian tumors and fimbria control Refer to individual Series

2012-02-16 | E-GEOD-28979 | biostudies-arrayexpress

Wild Type Tumor Repressor Protein 53 (TRP53) Promotes Ovarian Cancer Cell survival

Project description:Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated expression of wild type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53-) mice. By comparing morphology and gene expression profiles in the Trp53+ and Trp53- OSE cells, we document that wild-type TRP53 acts as a major promoter of OSE cell survival and differentiation: cells lacking Trp53 are transformed yet are less adherent, migratory and invasive and exhibit a gene expression profile more like normal OSE cells. These results provide a new paradigm: wild type TRP53 does not preferentially induce apoptotic or senescent related genes in the Pten;Kras(Trp53+) cancer cells but rather increases genes regulating DNA repair, cell cycle progression and proliferation and decreases putative tumor suppressor genes. However, if TRP53 activity is forced higher by exposure to nutlin-3a (an MDM2 antagonist), TRP53 suppresses DNA repair genes and induces the expression of genes that control cell cycle arrest and apoptosis. Thus, in the Pten;Kras(Trp53+) mutant mouse OSE cells and likely in human TP53+ low grade ovarian cancer cells, wild type TRP53 controls global molecular changes that are dependent on its activation status. These results suggest that activation of TP53 may provide a promising new therapy for managing type I ovarian cancer and other cancers in humans where wild-type TP53 is expressed. A direct comparison of ovarian surface epithelia cells from three different genotype mice

2012-06-20 | E-GEOD-34882 | biostudies-arrayexpress

Gene expression analysis of human serious ovarian tumors and fimbria control

2012-02-16 | GSE28721 | GEO

Gene expression analysis of ovarian tumors from mice with knockout of DICER and PTEN

2012-02-16 | GSE28720 | GEO

Pten loss and RAS/MAPK activation cooperate to promote EMT and prostate cancer metastasis initiated from stem/progenitor cells

Project description:PTEN loss or PI3K/AKT signaling pathway activation correlates with human prostate cancer progression and metastasis. However, in preclinical murine models, deletion of Pten alone fails to mimic the significant metastatic burden that frequently accompanies the end stage of human disease. To identify additional pathway alterations that cooperate with PTEN loss in prostate cancer progression, we surveyed human prostate cancer tissue microarrays and found that the RAS/MAPK pathway is significantly elevated both in primary and metastatic lesions. In an attempt to model this event, we crossed conditional activatable K-rasG12D/WT mice with the prostate conditional Pten deletion model we previously generated. Although RAS activation alone cannot initiate prostate cancer development, it significantly accelerated progression caused by PTEN loss, accompanied by epithelial-to-mesenchymal transition (EMT) and macrometastasis with 100% penitence. A novel stem/progenitor subpopulation with mesenchymal characteristics was isolated from the compound mutant prostates, which was highly metastatic upon orthotopic transplantation. Importantly, inhibition of RAS/MAPK signaling by PD325901, a MEK inhibitor, significantly reduced the metastatic progression initiated from transplanted stem/progenitor cells. Collectively, these data indicate that activation of RAS/MAPK signaling serves as a potentiating second hit to alteration of the PTEN/PI3K/AKT axis and co-targeting both pathways is highly effective in preventing the development of metastatic prostate cancers. Murine mutants with prostate specific loss of Pten and K-ras activation (K-rasG12D) under regulation of the probasin promoter developed high grade, invasive prostate cancer. RNA was extracted from dissected prostate lobes from individual mutants with pathology thought to closely mimic human disease. Prostate tissue was subject to RNA extraction and hybridization on Affymetrix cDNA microarrays.

2012-02-28 | E-GEOD-34839 | biostudies-arrayexpress

Gene expression profile at single cell level from the dorsal skin of WT and Tsk mice [bulk RNA-seq]

Project description:Patients with systemic sclerosis have a significantly increased incidence of developing various solid malignancies within a few years of systemic sclerosis onset but the mechanism of tumor promotion is not well understood. The tight skin (TSK) mouse has been a valuable model for investigating systemic sclerosis-related pathologies due to increased extracellular matrix deposition, fibrosis in connective tissues, and altered immune cell activation. Despite the role of extracellular matrix and fibrosis in cancer progression, the potential of the TSK mouse as a model for cancer studies is unexplored. Our RNA sequencing analysis of adult dorsal skin samples from TSK and wild-type (WT) mice revealed a notable enrichment for genes typically associated with cancer aggressiveness and desmoplasia. To investigate the impact of the altered microenvironment in TSK mice on cancer progression, we compared the tumor-forming capabilities in TSK mice and WT mice using a syngeneic mouse model of ovarian cancer. TSK mice exhibited larger and more invasive subcutaneous and intraperitoneal tumors in comparison to WT controls, suggesting the role of the microenvironment in promoting cancer progression. Single-cell RNA sequencing analysis of tumors in TSK and WT mice revealed a higher neutrophil-to-lymphocyte ratio, and an enrichment in profibrotic subpopulations of myofibroblasts and macrophages in TSK mice.

2024-04-08 | GSE255493 | GEO

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