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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE36565 | GEO | 2013/03/22

SECONDARY ACCESSION(S): PRJNA153719

REPOSITORIES: GEO

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Project description:Purpose: There is a quest for novel non-invasive diagnostic markers for the detection of breast cancer. The goal of this study is to identify circulating microRNA signatures using a cohort of Asian Chinese breast cancer patients, and to compare microRNA profiles between tumour and serum samples. Experimental design: MicroRNAs from paired breast cancer tumours, normal tissue and serum samples derived from 32 patients were comprehensively profiled using microarrays (1300 microRNAs against tumour and normal tissues) or LNA RT-PCR panels (742 microRNAs against serum samples). Serum samples from healthy individuals (n=22) were also employed as normal controls. Significant serum microRNAs, identified by logistic regression, were validated in an independent set of serum samples from patients (n=82) and healthy controls (n=53). Results: The 20 most significant microRNAs differentially expressed in breast cancer tumours included miR-21, miR-10b, and miR-145, previously shown to be dysregulated in breast cancer. Interestingly, 16 of the 20 most significant microRNAs differentially expressed in serum samples were novel. MiR-1, miR-92a, miR-133a and miR-133b were identified as the most important diagnostic markers, and were successfully validated; receiver operating characteristic curves derived from combinations of these microRNAs exhibited areas under the curves of 0.944-0.946. Only seven microRNAs were overexpressed in both tumours and serum, suggesting that microRNAs may be released into the serum selectively. Conclusion: The clinical employment of microRNA signatures as a non-invasive diagnostic strategy is promising, but should be further validated for different subtypes of breast cancers. "_A" and "_B" are two tissue sections of the same sample; "_1" and "_2" represents 2 runs of the same sample; na = not available All tissue samples were histologically confirmed by a pathologist using hematoxylin and eosin staining of cryosectioned specimens. One tumour sample was rejected due to failure to detect any tumour cells. Except for two samples (with 30% and 40% tumour cells), all tumour tissues employed had a minimum of 60% tumour cells, as estimated microscopically. Overall, the breast cancer tumour samples had an average of 71% tumour cells. The criteria for adjacent normal tissue were absence of tumour cells and presence of epithelial cells. Hence, after histological confirmation, 31 breast cancer tumours and 23 matched normal tissues were employed for microRNA extraction and profiling using microarray.

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Whole genome expression after modulation of miR-30a expression

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