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Cell density, Her2 and progesterone signaling regulate dissemination of breast cancer cells

ABSTRACT: Cell density, Her2 and progesterone signaling regulate dissemination of breast cancer cells

PROVIDER: PRJNA283387 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2014740.fastq.gz	Fastqsanger.gz
	SRR2014731.fastq.gz	Fastqsanger.gz
	SRR2014741.fastq.gz	Fastqsanger.gz
	SRR2014732.fastq.gz	Fastqsanger.gz
	SRR2014742.fastq.gz	Fastqsanger.gz

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Cell density, Her2 and progesterone signaling regulate dissemination of breast cancer cells [Gene expression]

Project description:Disseminated breast cancer cells display genotypes disparate from the predominant clone of the primary tumor before manifestation of metastasis, suggesting that cancer cell dissemination occurs preferentially early; however, the underlying molecular mechanisms are unknown. Investigating metastasis in a Her2-driven mouse model, we found that the progesterone-induced paracrine cytokines Wnt4 and Rankl induced migration and early dissemination shortly after Her2 activation. Once tumorigenic growth was established, progesterone receptor (PgR) expression was lost and Wnt4/Rankl induced proliferation. The altered response from migration to proliferation was determined by cell density involving miRNA-regulated PgR expression and was reversible. Cells from early, low-density lesions displayed more functional stemness traits than cells from dense, advanced tumors, migrated more and founded significantly more metastases. The data suggest that many metastases are derived from early-disseminated cancer cells, implying that our concepts for systemic therapy need to be revised.

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Project description:Breast cancer is a heterogeneous disease encompassing a number of phenotypically diverse tumours. Expression levels of the estrogen, progesterone and HER2/neu receptors which characterise clinically distinct breast tumors have been shown to change during disease progression and in response to systemic therapies. Mi(cro)RNAs play critical roles in diverse biological processes and are aberrantly expressed in several human neoplasms including breast cancer, where they function as regulators of tumour behaviour and progression. The aims of this study were to identify miRNA signatures that accurately predict the oestrogen receptor (ER), progesterone receptor (PR) and HER2/neu receptor status of breast cancer patients to provide insight into the regulation of breast cancer phenotypes and progression. Expression profiling of 353 microRNAs was performed in 29 early stage breast cancer specimens. MiRNA signatures associated with ER, PR and HER2/neu status were generated using artificial neural networks (ANN) and expression of specific microRNAs was validated using RQ-PCR. Results: Stepwise artificial neural network (ANN) analysis identified predictive miRNA signatures corresponding with estrogen (miR-342, miR-299, miR-217, miR -190, miR-135b, miR-218), progesterone (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and HER2/neu (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) receptor status. MiR-342 and miR-520g expression was further analysed in 95 breast tumours. MiR-342 expression was highest in ER and HER2/neu positive luminal B tumours and lowest in triple-negative tumours. MiR-520g expression was elevated in ER and PR negative tumours.

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