Expression analysis of ovarian cancer cell line
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE84723 | GEO | 2016/07/23
SECONDARY ACCESSION(S): PRJNA330949
REPOSITORIES: GEO
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Project description:The aim of this analysis is searching the target gene of miR-135a-3p in ovarian cancer cell line. The gene expression of cell line with overexpressed miR-blank or miR-135a-3p was compared. Three ovarian cancer cell lines were enrolled this study. Those cells were transfected with miR-blank as control or miR-135a-3p.
2016-07-23 | E-GEOD-84723 | biostudies-arrayexpress
Project description:Background: The aim of this study was to identify differentially expressed miRNAs in high-grade serous ovarian carcinoma (HGSC), clear cell ovarian carcinoma (CCC) and ovarian surface epithelium (OSE). Selected miRNAs were evaluated for association with clinical parameters including survival, and miRNA/mRNA interactions were mapped. Results: Differentially expressed miRNAs between HGSC, CCC and OSE were identified, of which 18 were validated (p<0.01) using RT-qPCR in an extended cohort. Compared with OSE, miR-205-5p was the most overexpressed miRNA in HGSC. miR-200 family members and miR-182-5p were the most overexpressed in HGSC and CCC compared with OSE, whereas miR-383 was the most underexpressed. miR-509-3-5p, miR-509-5p, miR-509-3p and miR-510 were among the strongest differentiators between HGSC and CCC, all being significantly overexpressed in CCC compared with HGSC. High miR-200c-3p expression was associated with poor progression-free (p=0.031) and overall (p=0.026) survival in HGSC. Interacting miRNAs and mRNA targets, including those of a TP53-related pathway presented previously, were identified in HGSC. Conclusions: Several miRNAs are overexpressed in HGSC and CCC compared with OSE, including the miR-200 family, among which miR-200c-3p is associated with survival in HGSC. A set of miRNAs differentiates CCC from HGSC, of which miR-509-3-5p and miR-509-5p are the strongest classifiers. Several interactions between miRNAs and mRNAs in HGSC were mapped. Methods: Differences in miRNA expression between HGSC, CCC and OSE scrapings were analyzed by global miRNA expression profiling (Affymetrix GeneChip miRNA 2.0 Arrays, n=30), validated by RT-qPCR (n=63), and evaluated for associations with clinical parameters. For HGSC, differentially expressed miRNAs were linked to differentially expressed mRNAs identified previously (GSE36668).
2014-02-13 | E-GEOD-47841 | biostudies-arrayexpress
Project description:Background: The aim of this study was to identify differentially expressed miRNAs in high-grade serous ovarian carcinoma (HGSC), clear cell ovarian carcinoma (CCC) and ovarian surface epithelium (OSE). Selected miRNAs were evaluated for association with clinical parameters including survival, and miRNA/mRNA interactions were mapped. Results: Differentially expressed miRNAs between HGSC, CCC and OSE were identified, of which 18 were validated (p<0.01) using RT-qPCR in an extended cohort. Compared with OSE, miR-205-5p was the most overexpressed miRNA in HGSC. miR-200 family members and miR-182-5p were the most overexpressed in HGSC and CCC compared with OSE, whereas miR-383 was the most underexpressed. miR-509-3-5p, miR-509-5p, miR-509-3p and miR-510 were among the strongest differentiators between HGSC and CCC, all being significantly overexpressed in CCC compared with HGSC. High miR-200c-3p expression was associated with poor progression-free (p=0.031) and overall (p=0.026) survival in HGSC. Interacting miRNAs and mRNA targets, including those of a TP53-related pathway presented previously, were identified in HGSC. Conclusions: Several miRNAs are overexpressed in HGSC and CCC compared with OSE, including the miR-200 family, among which miR-200c-3p is associated with survival in HGSC. A set of miRNAs differentiates CCC from HGSC, of which miR-509-3-5p and miR-509-5p are the strongest classifiers. Several interactions between miRNAs and mRNAs in HGSC were mapped.
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Project description:MicroRNAs (miRNAs) are a class of endogenous small non-coding RNAs. They act as negative regulators of protein-coding gene expression at the post-transcriptional level via sequence-specific interaction with the 3' UTR of targeted mRNAs. A miR-135a dysregulation has been observed in various cancers, where a dual role of oncomiR or of tumor suppressor has been reported for the cancers profiled to date; however, knowledge is limited to explain these contentious data. In the present study, we investigate the regulation and mechanism of action of miR-135a, including identification of functionally targets that contributes to its actions, in prostate cancer progression. We demonstrate that the expression of miR-135a is regulated by androgens, in a time- and dose-dependent manner and identify miR-135a as a direct target gene of the androgen receptor AR. A functional androgen response element (ARE) is identified in the promoter region of the miR-135a gene and ChIP assay reveal AR protein binding to. Anti-androgen treatment and AR-targeted siRNA knockdown strategy suggest a novel function for miR-135a in AR signaling. In silico prediction, transcriptomic and proteomic combined analyses lead to identify ROCK-1/-2 as two miR-135a-targeted genes. Luciferase reporter assays indicate that these two proteins are miR-135a's direct targets. We finally demonstrate that miR-135a acts through ROCK-1/-2 pathways to affect migration and invasion cellular processes. MiR-135a expression level was lower in surgical cancerous samples compared to paired adjacent non-tumoral tissues and was gradually diminished consistent with cancer progression, suggesting the significance of miR-135a-mediated prostate cancer transformation. Our findings define miR-135a as a candidate tumor suppressor and potential prognostic marker in human prostate cancer.
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Project description:MicroRNAs (miRNAs) are a class of endogenous small non-coding RNAs. They act as negative regulators of protein-coding gene expression at the post-transcriptional level via sequence-specific interaction with the 3' UTR of targeted mRNAs. A miR-135a dysregulation has been observed in various cancers, where a dual role of oncomiR or of tumor suppressor has been reported for the cancers profiled to date; however, knowledge is limited to explain these contentious data. In the present study, we investigate the regulation and mechanism of action of miR-135a, including identification of functionally targets that contributes to its actions, in prostate cancer progression. We demonstrate that the expression of miR-135a is regulated by androgens, in a time- and dose-dependent manner and identify miR-135a as a direct target gene of the androgen receptor AR. A functional androgen response element (ARE) is identified in the promoter region of the miR-135a gene and ChIP assay reveal AR protein binding to. Anti-androgen treatment and AR-targeted siRNA knockdown strategy suggest a novel function for miR-135a in AR signaling. In silico prediction, transcriptomic and proteomic combined analyses lead to identify ROCK-1/-2 as two miR-135a-targeted genes. Luciferase reporter assays indicate that these two proteins are miR-135a's direct targets. We finally demonstrate that miR-135a acts through ROCK-1/-2 pathways to affect migration and invasion cellular processes. MiR-135a expression level was lower in surgical cancerous samples compared to paired adjacent non-tumoral tissues and was gradually diminished consistent with cancer progression, suggesting the significance of miR-135a-mediated prostate cancer transformation. Our findings define miR-135a as a candidate tumor suppressor and potential prognostic marker in human prostate cancer.
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