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Mesenchymal cancer cell-stromal crosstalk promotes niche activation, epithelial reversion and metastatic colonization

ABSTRACT: The experiment was design to address the intrinsic differences between metastatic cancer stem cells in the primary tumour and during metastatic colonization in the mouse mammary gland tumour model MMTV-pyMT.

ORGANISM(S): Mus musculus

PROVIDER: GSE63558 | GEO | 2015/11/21

SECONDARY ACCESSION(S): PRJNA268205

REPOSITORIES: GEO

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Mesenchymal cancer cell-stromal crosstalk promotes niche activation, epithelial reversion and metastatic colonization

Project description:The experiment was design to address the intrinsic differences between metastatic cancer stem cells in the primary tumour and during metastatic colonization in the mouse mammary gland tumour model MMTV-pyMT. Total RNA was prepared from the indicated cancer cells freshly isolated, stained and FACS sorted either from primary tumours or from lungs upon intravenous injection of cancer cells.

2015-11-21 | E-GEOD-63558 | biostudies-arrayexpress

Mesenchymal Cancer Cell-Stroma Crosstalk Promotes Niche Activation, Epithelial Reversion, and Metastatic Colonization.

Project description: Not available

| S-EPMC4695340 | biostudies-literature

Comparative transcriptome analysis of metastatic heterogeneity in a mouse model of breast cancer

Project description:We aimed to understand the transcriptome patterns of organ-derived cancer cell isolates from MMTV-PyMT mice. Tissues from primary tumors and organs harboring distal metastases were harvested from cancer bearing female mice. Although metastatic progression from primary tumors to lung tissue is well studied in the MMTV-PyMT model, metastases to other distal organs and the significance of intratumor heterogeneity across metastases from distal organs remain unclear. To gain insight, we established an array of metastatic cell lines harvested from the MMTV-PyMT breast cancer mouse model. Sequencing at bulk and single-cell level were performed and used to examine the effects of cell heterogeneity on metastases and organ tropism

2021-04-01 | GSE165393 | GEO

Expression data from MMTV-PyMT Induced Tumors

Project description:Loss of E2F transcription factos alters metastatic capacity of MMTV-PyMT tumors. We used microarrays to futher characterize the effects of E2F loss on mammary tumorigenesis in MMTV-PyMT mice.

2018-02-22 | GSE104397 | GEO

SMAD4 represses FOSL1 expression and pancreatic cancer metastatic colonization

Project description:Less than 8% of patients diagnosed with pancreatic ductal adenocarcinomas (PDAC) survive more than five years in part due to late stage diagnosis. Approximately half of PDAC patients exhibit loss of SMAD4, which correlates with increased metastatic disease. Here we demonstrate that SMAD4 is a suppressor of metastatic colonization. Using isogenic human PDAC cell lines expressing or lacking SMAD4, both in vitro and in vivo, we define SMAD4-dependent gene expression changes in metastatic lesions. We performed a pooled in vivo open reading frame (ORF) screen of SMAD4 transcriptional targets and identified genes that, induce tumor seeding and growth at secondary sites. We found that expression of the transcription factor FOSL1 was sufficient to drive metastatic colonization. SMAD4 directly binds and represses the activity of the FOSL1 enhancer. These studies demonstrate a direct role for SMAD4 in regulating metastatic colonization and identify FOSL1 as a SMAD4-regulated gene involved in PDAC progression.

2021-08-02 | GSE148248 | GEO

SSeCKS/Akap12 suppresses metastatic melanoma lung colonization by attenuating Src-mediated pre-metastatic niche crosstalk.

Project description: Not available

| S-EPMC6173366 | biostudies-literature

Temporal multi-omics identifies LRG1 as vascular instructor of early metastatic colonization.

Project description:Metastasis is the primary cause of cancer-related mortality and the mechanistically least well understood step of the tumor progression cascade. Employing surgical preclinical metastasis models, we show here that small primary tumors reprogram the body’s vascular endothelium to alter systemic homeostasis and to condition the premetastatic niche for metastatic colonization. Endothelial cells thereby serve as an amplifier of tumor-induced instructive signals. The combined endothelial transcriptomic and serum proteomic screen identified the TGFß pathway signaling specifier LRG1 as an early vascular niche instructor of metastatic colonization. Adjuvant LRG1 inhibition to primary tumor-resected mice delayed metastatic growth and increased overall survival. The study has thereby established the premetastatic systems map of primary tumor-induced vascular changes and identified LRG1 as a therapeutic target for metastasis

2022-05-16 | PXD013978 | Pride

Monocytes from peripheral blood from mouse with and without tumour

Project description:Monocytes from peripheral blood of tumour-bearing (B6Tg(MMTV-PyMT)634Mul/Lellj) or non-tumor-bearing C57BL/6JCrl mice were FACS sorted and single cells analysed by SMARTseq2

2023-06-30 | GSE183838 | GEO

Monocytes from peripheral blood from mouse with and without tumour II

Project description:Monocytes from peripheral blood of tumour-bearing (B6Tg(MMTV-PyMT)634Mul/Lellj) or non-tumor-bearing C57BL/6JCrl mice were FACS sorted and single cells analysed by SMARTseq2

2022-02-09 | GSE184870 | GEO

Autophagic turnover of NBR1 restricts metastatic colonization during mammary tumor progression

Project description:Autophagy is implicated in promoting the metastatic potential of tumor cells. Utilizing a mouse model of mammary cancer to temporally delete essential autophagy regulators, ATG12 or ATG5, in tumor cells during distinct stages of carcinoma progression, we determine a stage-specific role for autophagy in suppressing metastatic colonization. In stark contrast to the tumor-promoting role of autophagy in primary mammary tumors, autophagy restricts colonization of disseminated tumor cells (DTCs) and prevents the acquisition of basal epithelial characteristics, effects that are dependent on turnover of the autophagy-specific substrate, Neighbor to BRCA1 (NBR1). Analysis of human breast cancer samples corroborates the importance of NBR1 in overall survival and metastasis, highlighting NBR1 as a potential therapeutic target in preventing DTCs from developing into overt, clinical disease.

2020-02-19 | GSE124209 | GEO

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