Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Whole genome expression after modulation of miR-30a expression

ABSTRACT: A subset of breast cancer cells displays increased ability to self-renew and reproduce breast cancer heterogeneity (so called, breast tumour-initiating cells or BT-ICs). As microRNAs (miRNAs) control developmental programs in stem cells, BT-ICs may also rely on specific miRNA profiles for their sustained activity. We analyzed miRNA expression in a model of putative BT-ICs and found that miR-30 family regulates growth under “stemness” conditions. A target screening revealed that miR-30 family modulates the expression of apoptosis and proliferation-related genes. The importance of miR-30 in tumour progression and breast cancer stemness was demonstrated in vivo using a mouse mammary cancer model. This is the first analysis of target prediction in a whole family of microRNAs potentially involved in survival of putative BT-ICs. Total RNA from cells transfected with Pre-miR-30 and KD-miR-30 family and control KD-miR-159 was extracted and reverse-transcribed and hybrized on HT12 Human bead chips

ORGANISM(S): Homo sapiens

SUBMITTER: Hector Hernandez-Vargas

PROVIDER: E-GEOD-36565 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MicroRNA miR-30 family regulates non-attachment growth of breast cancer cells.

Ouzounova Maria M Vuong Tri T Ancey Pierre-Benoit PB Ferrand Mylène M Durand Geoffroy G Le-Calvez Kelm Florence F Croce Carlo C Matar Chantal C Herceg Zdenko Z Hernandez-Vargas Hector H

BMC genomics 20130228

<h4>Background</h4>A subset of breast cancer cells displays increased ability to self-renew and reproduce breast cancer heterogeneity. The characterization of these so-called putative breast tumor-initiating cells (BT-ICs) may open the road for novel therapeutic strategies. As microRNAs (miRNAs) control developmental programs in stem cells, BT-ICs may also rely on specific miRNA profiles for their sustained activity. To explore the notion that miRNAs may have a role in sustaining BT-ICs, we perf ...[more]

PMID: 23445407

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Project description:Introduction: Amplification at chromosome 8q24 is one of the most frequent genomic abnormalities in human cancers and is associated with reduced survival duration in breast and ovarian cancers. The minimal amplified region encodes c-MYC and the non-coding RNA, PVT1 including miR-1204 encoded in exon 1b. Here we analyzed the genomic changes at chromosome 8q24.21 in breast cancer and the functional roles of miR-1204 in breast and ovarian cancer progression. Methods: The genomic changes at chromosome 8q24.21 were detected in 997 breast cancer tumors and 40 breast cancer cell lines. Expression of miR-1204 in breast and ovarian cancer cell lines was investigated by qRT-PCR method. The role of miR-1204 in the tumorigenesis of breast and ovarian cancer was explored using both knockdown and overexpression of miR-1204 in vitro. Candidate miR-1204 target genes from two independent expression microarray datasets and computational predict programs were identified and further validated by qRT-PCR and western blot methods. The role of inhibition of miR-1204 on tamoxifen sensitivity in breast cancer cells was also investigated. Results: MiR-1204 is frequently co-amplified with MYC and expression of miR-1204 is strongly correlated with the expression and amplification of the noncoding PVT1 transcript and less so with MYC in human breast and ovarian cancer cells. Inhibition of miR-1204 decreases cell proliferation and increased apoptosis in breast and ovarian cancer cell lines with 8q24 amplification, but not in lines without amplification and so may be involved in Myc-induced apoptosis. Additionally, overexpression of miR-1204 enhances both breast and ovarian cancer cell growth and Myc-initiated Rat1A cell transformation. Computational and experimental analyses 30 promising candidate miR-1204 target genes. mRNA levels for these genes were assessed after over expression and knockdown of miR-1204 as were protein levels for 10 genes for which antibodies were available. These studies implicated VDR and ESR1 as miR-1204 targets. Inhibition of miR-1204 increased response to tamoxifen in Estrogen Receptor negative breast cancer cell lines. Conclusions: We conclude that amplification of miR-1204 contributes to breast and ovarian pathophysiology at least in part, by increasing proliferation and down regulating apoptosis and by decreasing expression of VDR and ESR1. Seven cell line sample pairs, where samples are LNA transfected with antimiR-1204 or antimiR-1204 control

Dataset Information

Whole genome expression after modulation of miR-30a expression

Publications

MicroRNA miR-30 family regulates non-attachment growth of breast cancer cells.

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