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Targeting IRAK2 in triple-negative breast cancer cells decreases cellular growth in vitro and delays tumor progression in murine models

ABSTRACT: Targeting IRAK2 in triple-negative breast cancer cells decreases cellular growth in vitro and delays tumor progression in murine models

PROVIDER: PRJNA879863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21537365.fastq.gz	Fastqsanger.gz
	SRR21537366.fastq.gz	Fastqsanger.gz
	SRR21537367.fastq.gz	Fastqsanger.gz
	SRR21537368.fastq.gz	Fastqsanger.gz
	SRR21537369.fastq.gz	Fastqsanger.gz

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Targeting IRAK2 in triple-negative breast cancer cells decreases cellular growth in vitro and delays tumor progression in murine models

Project description:Breast cancer stem cells (BCSCs) are responsible for tumor recurrence and therapy resistance. We have established primary BCSC cultures from human tumors of triple-negative breast cancer (TNBC), a subgroup of breast cancer likely driven by BCSCs. Primary BCSCs generate xenografts phenocopying the tumors of origin, representing a suitable model to investigate breast cancer targeting strategies. In the TNBC cell line MDA-MB-468, we previously screened kinases whose depletion elicited a differentiation response, among which IRAK2 was identified. Since IRAK2 is highly enriched in primary BCSCs we wondered if its depletion could affect their growth. Primary BCSCs and MDA-MB-468 presenting IRAK2 downregulation exhibited decreased proliferation and sphere-forming capacity, evidencing the role of IRAK2 in cellular growth and self-renewal. When transplanted orthotopically into immunocompromised mice, IRAK2 knockdown cells originated smaller xenografts in comparison with control cells, suggesting that IRAK2 downregulation may delay tumor development. Investigating the molecular pathways affected by the knockdown, NF-κB and ERK phosphorylation, IL-6 and cyclin D1 expression, ERN1 signaling and autophagy were decreased in a cell line-dependent way. Transcriptome analysis confirmed that the cells were to some extent differently affected by the knockdown, indicating that their heterogeneity, different mutations, genetic background, expression of IRAK2 and level of its downregulation could influence the outcome of the knockdown. Given that overall IRAK2 downregulation decreased cellular ability to sustain aggressive growth and to endure cellular stress, IRAK2 may be considered an interesting target to compromise TNBC progression, positively contributing to TNBC clinical outcome.

2022-09-15 | GSE213228 | GEO

IRAK2 Downregulation in Triple-Negative Breast Cancer Cells Decreases Cellular Growth In Vitro and Delays Tumour Progression in Murine Models.

Project description:Breast cancer stem cells (BCSCs) are responsible for tumour recurrence and therapy resistance. We have established primary BCSC cultures from human tumours of triple-negative breast cancer (TNBC), a subgroup of breast cancer likely driven by BCSCs. Primary BCSCs produce xenografts that phenocopy the tumours of origin, making them an ideal model for studying breast cancer treatment options. In the TNBC cell line MDA-MB-468, we previously screened kinases whose depletion elicited a differentiation response, among which IRAK2 was identified. Because primary BCSCs are enriched in IRAK2, we wondered whether IRAK2 downregulation might affect cellular growth. IRAK2 was downregulated in primary BCSCs and MDA-MB-468 by lentiviral delivery of shRNA, causing a decrease in cellular proliferation and sphere-forming capacity. When orthotopically transplanted into immunocompromised mice, IRAK2 knockdown cells produced smaller xenografts than control cells. At the molecular level, IRAK2 downregulation reduced NF-κB and ERK phosphorylation, IL-6 and cyclin D1 expression, ERN1 signalling and autophagy in a cell line-dependent way. Overall, IRAK2 downregulation decreased cellular aggressive growth and pathways often exploited by cancer cells to endure stress; therefore, IRAK2 may be considered an interesting target to compromise TNBC progression.

| S-EPMC9917074 | biostudies-literature

Mutagenesis sensitizes murine models of triple negative breast cancer to immunotherapy

Project description:This study identifies mechanisms of response to immune checkpoint inhibition in mouse models of triple negative breast cancer.

2019-11-13 | GSE136206 | GEO

Mutagenesis sensitizes murine models of triple negative breast cancer to immunotherapy

Project description:Mutagenesis sensitizes murine models of triple negative breast cancer to immunotherapy

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The BET-bromodomain inhibitor OTX015 (MK-8628) exerts in vitro and in vivo anti-tumor activity in triple-negative breast cancer models as single agent and in combination with everolimus

Project description:assess the efficacy of OTX015 (MK-8628) BET inhibitor in vitro and in vivo triple negative breast cancer models

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Macrophage reponse to triple-negative breast cancer cells in vitro

Project description:Gene expression profiling of monocyte-derived macrophage polarised by triple-negative breast cancer cell conditioned medium

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Development and Characterization of Syngeneic Orthotopic Transplant Models of Obesity-Responsive Triple-Negative Breast Cancer in C57BL/6J Mice (in vitro)

Project description:To develop transplantable triple-negative breast cancer cell lines from spontaneous mammary tumors arising C3(1)/SV40 T-antigen (C3-TAg) transgenic C57BL6 mice.

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Yale Triple Negative Breast Cancer Cohort

Project description:Triple negative breast cancer (TNBC) is characterized by high proliferation, poor differentiation and a poor prognosis due to high rates of recurrence. Despite lower overall incidence African American (AA) patients suffer from higher breast cancer mortality in part due to the higher proportion of TNBC cases among AA patients compared to European Americans (EA). It was recently shown that the clinical heterogeneity of TNBC is reflected by distinct transcriptional programs with distinct drug response profiles in preclinical models. In this study, we used gene expression profiling and immunohistochemistry to eluicidate potential differences between TNBC tumors of EA and AA patients on a molecular level. WG-DASL experiment of 90 FFPE samples of ER, PR and HER2 (triple) negative breast cancer samples diagnosed between 1987 and 2007. Invasive disease was identified on H&E sections by the study pathologist and one to three 1.5 mm cores were punched from the top down in the designated tumor areas of each FFPE block. The cores were deparaffinized with xylene at 50°C for 3 minutes. RNA was extracted using the RecoverAll Total Nucleic Acid Isolation kit (Applied Biosystems) following the manufacturer's protocol. The isolated RNA was hybridized to Whole-Genome DASL (HumanRef8 V 3.0, Illumina) at the Yale Center for Genome Analysis. 90 primary tumor RNA samples from 90 patients were adequate for analysis and passed Quality control.

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Pax3 loss of function delays tumor progression in kRAS-induced zebrafish rhabdomyosarcoma models

Project description:Pax3 loss of function delays tumor progression in kRAS-induced zebrafish rhabdomyosarcoma models

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Establishment of EGFR-inhibitor resistant triple negative breast cancer models from patient derived xenografts

Project description:Establishment of EGFR-inhibitor resistant triple negative breast cancer models from patient derived xenografts

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