Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA309419 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We found a novel molecular link between hyperglycaemia and the increased frequency of aggressive prostate cancer. High glucose was demonstrated to increase the expression of miR-301a which targeted Smad4 and p21, resulted in promoting the proliferation of prostate cancer cells.
2016-01-22 | GSE77092 | GEO
Project description:The epidemiologic association between statin use and decreased risk of advanced prostate cancer suggests that statins may inhibit prostate cancer development and/or progression. Studies were performed to determine the effects of a model statin, atorvastatin (ATO), on the proliferation and differentiation of prostate cancer cells, and to identify possible mechanisms of ATO action. ATO inhibited the in vitro proliferation of both LNCaP and PC3 human prostate cancer cells in dose-dependent fashion. The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in that cell line, as demonstrated by increased expression of LC3-II. miR-182 was consistently upregulated by ATO in PC3 cells, but not in LNCaP cells. ATO upregulation of miR-182 in PC3 cells was p53-independent and was reversed by geranylgeraniol. Transfection of miR-182 inhibitors decreased expression of miR-182 by >98% and attenuated the antiproliferative activity of ATO. miR-182 expression in PC3 cells was also increased in response to stress induced by serum withdrawal, suggesting that miR-182 upregulation can occur due to nutritional stress. Bcl2 and p21 were identified to be potential target genes of miR-182 in PC3 cells. Bcl2 was downregulated and p21 was upregulated in PC3 cells exposed to ATO. These data suggest that miR-182 may be a stress-responsive miRNA that mediates ATO action in prostate cancer cells. Gene and miRNA expression in two prostate cancer cell lines treated with Atorvastatin vs. untreated control.
2013-09-30 | E-GEOD-46375 | biostudies-arrayexpress
Project description:The epidemiologic association between statin use and decreased risk of advanced prostate cancer suggests that statins may inhibit prostate cancer development and/or progression. Studies were performed to determine the effects of a model statin, atorvastatin (ATO), on the proliferation and differentiation of prostate cancer cells, and to identify possible mechanisms of ATO action. ATO inhibited the in vitro proliferation of both LNCaP and PC3 human prostate cancer cells in dose-dependent fashion. The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in that cell line, as demonstrated by increased expression of LC3-II. miR-182 was consistently upregulated by ATO in PC3 cells, but not in LNCaP cells. ATO upregulation of miR-182 in PC3 cells was p53-independent and was reversed by geranylgeraniol. Transfection of miR-182 inhibitors decreased expression of miR-182 by >98% and attenuated the antiproliferative activity of ATO. miR-182 expression in PC3 cells was also increased in response to stress induced by serum withdrawal, suggesting that miR-182 upregulation can occur due to nutritional stress. Bcl2 and p21 were identified to be potential target genes of miR-182 in PC3 cells. Bcl2 was downregulated and p21 was upregulated in PC3 cells exposed to ATO. These data suggest that miR-182 may be a stress-responsive miRNA that mediates ATO action in prostate cancer cells. Gene and miRNA expression in two prostate cancer cell lines treated with Atorvastatin vs. untreated control.
2013-09-30 | E-GEOD-46374 | biostudies-arrayexpress
Project description:The epidemiologic association between statin use and decreased risk of advanced prostate cancer suggests that statins may inhibit prostate cancer development and/or progression. Studies were performed to determine the effects of a model statin, atorvastatin (ATO), on the proliferation and differentiation of prostate cancer cells, and to identify possible mechanisms of ATO action. ATO inhibited the in vitro proliferation of both LNCaP and PC3 human prostate cancer cells in dose-dependent fashion. The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in that cell line, as demonstrated by increased expression of LC3-II. miR-182 was consistently upregulated by ATO in PC3 cells, but not in LNCaP cells. ATO upregulation of miR-182 in PC3 cells was p53-independent and was reversed by geranylgeraniol. Transfection of miR-182 inhibitors decreased expression of miR-182 by >98% and attenuated the antiproliferative activity of ATO. miR-182 expression in PC3 cells was also increased in response to stress induced by serum withdrawal, suggesting that miR-182 upregulation can occur due to nutritional stress. Bcl2 and p21 were identified to be potential target genes of miR-182 in PC3 cells. Bcl2 was downregulated and p21 was upregulated in PC3 cells exposed to ATO. These data suggest that miR-182 may be a stress-responsive miRNA that mediates ATO action in prostate cancer cells.
2013-09-30 | GSE46375 | GEO
Project description:The epidemiologic association between statin use and decreased risk of advanced prostate cancer suggests that statins may inhibit prostate cancer development and/or progression. Studies were performed to determine the effects of a model statin, atorvastatin (ATO), on the proliferation and differentiation of prostate cancer cells, and to identify possible mechanisms of ATO action. ATO inhibited the in vitro proliferation of both LNCaP and PC3 human prostate cancer cells in dose-dependent fashion. The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in that cell line, as demonstrated by increased expression of LC3-II. miR-182 was consistently upregulated by ATO in PC3 cells, but not in LNCaP cells. ATO upregulation of miR-182 in PC3 cells was p53-independent and was reversed by geranylgeraniol. Transfection of miR-182 inhibitors decreased expression of miR-182 by >98% and attenuated the antiproliferative activity of ATO. miR-182 expression in PC3 cells was also increased in response to stress induced by serum withdrawal, suggesting that miR-182 upregulation can occur due to nutritional stress. Bcl2 and p21 were identified to be potential target genes of miR-182 in PC3 cells. Bcl2 was downregulated and p21 was upregulated in PC3 cells exposed to ATO. These data suggest that miR-182 may be a stress-responsive miRNA that mediates ATO action in prostate cancer cells.
2013-09-30 | GSE46374 | GEO
Project description:The chromosome 8q21 locus, which contains NKX3.1 and microRNA (miR)-3622 family (miR-3622a/b), is a frequently deleted region in human prostate cancer. Thus, miR-3622 is proposed as a tumor suppressor in various cancers, including prostate cancer, but its role remains debatable. In the present study, we found that mature miR-3622b-3p expression was higher in human prostate cancer than in normal prostate, while expression of miR-3622a was downregulated in human prostate cancer. Also, miR-3622b-3p facelifted cell proliferation, migration and invasion, whereas miR-3622a-3p inhibited cell migration and invasion but not proliferation in human prostate cancer cells. To address the role of miR-3622 locus, we knockout (KO) endogenous miR-3622, including both miR-3622a/b, in various human prostate cancer cell lines. Our data showed that miR-3622 KO reduced cell proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo. Functional analysis revealed that miR-3622 regulated p53 downstream gene network, including p21, c-MYC, and AIFM2, to control the cell cycle and apoptosis. Furthermore, using CRISPR interference, miRNA/mRNA immunoprecipitation assay, and dual-luciferase assay, we identified AIFM2, a direct target gene of miR-3622b-3p, that is responsible for miR-3622 KO-induced apoptosis. Also, we established a miR-3622-AIFM2 axis that contributes to oncogenic function during tumor progression. In addition, miR-3622 KO inhibited the epithelial-mesenchymal transition via upregulation of vimentin involved in prostate cancer metastasis. Our results suggest that miR-3622b-3p is overexpressed in human prostate cancer and plays an oncogenic role in tumor progression and metastasis via repression of p53 signaling, especially through a miR-3622-AIFM2 axis. On the other hand, deletion of miR-3622 at 8q21 locus in human prostate cancer may reduce oncogenic effects on tumor progression and metastasis.
2022-06-15 | GSE179399 | GEO
Project description:Purpose: we used next generation sequencing to analyze gene expression profiles of hippocampus from WT and miR-301a-/- mice. The goals of this study are to compare the different gene expression profiles of hippocampus between WT and miR-301a-/- mice.
2022-01-28 | GSE194389 | GEO
Project description:Purpose: we used next generation sequencing to analyze gene expression profiles of pancreatic tissues from KrasG12D;Pdx1-Cre and miR-301a-/-;KrasG12D;Pdx1-Cre mice treated with caerulein. The goals of this study are to compare the different gene expression profiles of pancreatic tissue between KrasG12D;Pdx1-Cre and miR-301a-/-;KrasG12D;Pdx1-Cre mice treated with caerulein.
2021-06-11 | GSE176571 | GEO
Project description:Lung cancer is the leading cause of cancer-related deaths worldwide. Despite advancements and improvements in surgical and medical treatments, the survival rate of lung cancer patients remains frustratingly poor. Local control for early stage non-small cell lung cancer (NSCLC) has dramatically improved over the last decades for both operable and inoperable patients. However, the molecular mechanisms of NSCLC invasion leading to regional and distant disease spread remain poorly understood. Here we identify miR-224 to be significantly up-regulated in NSCLC tissues, in particular in resected NSCLC metastasis. Increased miR-224 expression promotes cell migration, invasion and proliferation by directly targeting the tumor suppressors, TNFAIP1 and SMAD4. In concordance with in vitro studies, mouse xenograft studies validated that miR-224 function as a potent oncomiR in NSCLC in vivo. Moreover, we found promoter hypomethylation and activated ERK signaling to be involved in the regulation of miR-224 expression in NSCLC. Up-regulated mir-224 thus facilitates tumor progression by shifting the equilibrium of the partially antagonist functions of SMAD4 and TNFAIP1 towards enhanced invasion and growth in NSCLC. Our findings indicate that targeting miR-224 could be effective in the treatment of certain lung cancer patients Oncogenic role of miR-224 in lung cancer
2015-07-01 | E-GEOD-64859 | biostudies-arrayexpress
Project description:Translational characterization of hepatic miR-301a as a biomarker for acute rejection in experimental and clinical liver transplantation
| PRJNA270826 | ENA