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Homo sapiens

ABSTRACT: RNA-sequencing (RNA-seq) in breast cancer cell lines after ectopic manipulation of miR-26a expression

PROVIDER: PRJNA187476 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR653048_1.fastq.gz	Fastqsanger.gz
	SRR653048_2.fastq.gz	Fastqsanger.gz
	SRR653049_1.fastq.gz	Fastqsanger.gz
	SRR653049_2.fastq.gz	Fastqsanger.gz
	SRR653050_1.fastq.gz	Fastqsanger.gz

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RNA-sequencing (RNA-seq) in breast cancer cell lines after ectopic manipulation of miR-26a expression

Project description:RNA sequencing technology has been carried out in order to evaluate mRNA expression changes after manipulation of miR-26a in both MCF-7 and MDA-MB-231 breast cancer cell lines. To evaluate the entire set of genes modulated by miR-26a in breast cancer, we performed RNA-seq after ectopic manipulation of this miRNA. We over-expressed miR-26a in MCF-7 epithelial cancer cell lines and also reduced its activity by stably transfecting MDA-MB-231 mesenchymal-like cancer cell lines with a specific sponge vector. GO terms and pathway enriched analysis of the transcripts that significantly change upon miR-26 ectopic manipulation implicates miR-26ab in cell cycle, apoptosis, cell spreading and cell adhesion in breast cancer

2016-06-30 | E-GEOD-43726 | biostudies-arrayexpress

RNA-sequencing (RNA-seq) in breast cancer cell lines after ectopic manipulation of miR-26a expression

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Homo sapiens

Project description:RNA-seq in breast cancer cell lines after manipulation of miR-23b expression

| PRJNA165157 | ENA

RNA-seq in breast cancer cell lines after manipulation of miR-23b expression

Project description:RNA sequencing technology has been carried out in order to evaluate mRNA expression changes after manipulation of miR-23b in both MCF-7 and MDA-MB-231 breast cancer cell lines

2013-05-01 | GSE37918 | GEO

Trastuzumab produces therapeutic actions by upregulating miR-26a and miR-30b in breast cancer cells

Project description:Objective: Trastuzumab has been used for the treatment of HER2-positive breast cancer (BC). However, a subset of BC patients exhibited resistance to trastuzumab therapy. Thus, clarifying the molecular mechanism of trastuzumab treatment will be beneficial to improve the treatment of HER2-positive BC patients. In this study, we identified trastuzumab-responsive microRNAs that are involved in the therapeutic effects of trastuzumab. Methods and results: RNA samples were obtained from HER2-positive (SKBR3 and BT474) and HER2-negetive (MCF7 and MDA-MB-231) cells with and without trastuzumab treatment for 6 days. Next, we conducted a microRNA profiling analysis using these samples to screen those microRNAs that were up- or downregulated only in HER2-positive cells. This analysis identified miR-26a and miR-30b as trastuzumab-inducible microRNAs. Transfecting miR-26a and miR-30b induced cell growth suppression in the BC cells by 40% and 32%, respectively. A cell cycle analysis showed that these microRNAs induced G1 arrest in HER2-positive BC cells as trastuzumab did. An Annexin-V assay revealed that miR-26a but not miR-30b induced apoptosis in HER2-positive BC cells. Using the prediction algorithms for microRNA targets, we identified cyclin E2 (CCNE2) as a target gene of miR-30b. A luciferase-based reporter assay demonstrated that miR-30b post-transcriptionally reduced 27% (p=0.005) of the gene expression by interacting with two binding sites in the 3’-UTR of CCNE2. Conclusion: In BC cells, trastuzumab modulated the expression of a subset of microRNAs, including miR-26a and miR-30b. The upregulation of miR-30b by trastuzumab may play a biological role in trastuzumab-induced cell growth inhibition by targeting CCNE2. We obtained microRNA expression profiles of breast cancer cell lines, MCF7, MDA-MB-231, SKBR3, and BT474, with or without trastuzumab (4microgram/mL) treatment.

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Discovering the miR-26a/targetome in prostate cancer cells

Project description:In this work, we showed that the re-expression of miR-26a in DU-145 prostate cancer cells restored the tumor suppressor activity of miR-26a. To discover the genes and pathways elicited by miR-26a re-expression, we used the miRNA pull out assay to capture and the Next Generation Sequencing to identify the miR-26a targets. Data showed that: i) miR-26a captured both non-coding and coding RNAs; ii) 46% of transcripts were putative miR-26a targets according to target prediction algorithms; iii) 21 pathways were significantly enriched and the “Pathway in Cancer” was among those comprising the largest number of genes, including BIRC5 that we experimentally validated. Accordingly, the detection of cell proliferation-related events showed that miR-26a exerted its tumor suppressor activity at several levels, by decreasing the survival, impairing the migration of tumor cells and by inducing both apoptosis and cell cycle block. In conclusion, we showed that the collection of miR-26a interacting transcripts (miR-26a/targetome) represented a fruitful platform to decipher the miR-26a-dependent gene expression networks. In perspective the availability of miRNA-specific and tumor-specific targetomes will allow the discovery of new druggable tumor genes and pathways.

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miR-26a regulate the extracellular vesicle secretion from prostate cancer cells via targeting PFDN4, CHORDC1 and SHC4

Project description:Extracellular vesicles (EVs) are known to be involved in inter-cellular communication during cancer progression, however, the biogenesis of EVs in cancer cells is not completely unveiled. It has been shown that microRNAs (miRNAs) regulated variety of physiological and pathological phenomena, thus, miRNAs could regulate the EV secretion. Here, we have performed high throughput miRNA-based screening to identify the regulators of EV secretion using ExoScreen assay. By this miRNA-based screening, we identified miR-26a, which was reported as tumor suppressive miRNA, was found to be an miRNA involved in EV secretion from prostate cancer (PCa) cells. To study the effect of miR-26a on gene expression in EV secretion, transcriptome analysis for miR-26a overexpressing PCa cell lines was performed.

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