Gene expression after knocking down of c-Met in breast cancer brain metastatic cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE74968 | GEO | 2016/03/01
SECONDARY ACCESSION(S): PRJNA302058
REPOSITORIES: GEO
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Project description:The purpose of this study is to identify the target genes of c-Met signaling in breast cancer brain metastasis. 231BrM/Dox/shMet and SKBrM3/Dox/shMet cells were treated with or without doxycycline for 48hrs.
2016-03-01 | E-GEOD-74968 | biostudies-arrayexpress
Project description:We found that RANKL, expressed by cancer cells or derived from exogenous sources, consistently induced human prostate, breast, kidney, lung and liver cancer cells to colonize or metastasize to bone in an animal model of cancer bone metastasis. RANK-mediated signaling established a premetastatic niche through a forward feedback loop by inducing RANKL and c-Met expression and downstream signaling via upregulation of master regulator transcription factors regulating EMT (Twist1, Slug, Zeb1, Zeb2), stem cells (Sox2, Myc, Oct3/4 and Nanog), neuroendocrine cells (Sox 9, HIF-1α and FoxA2) and osteomimicry (c-Myc/Max, Sox2, Sox9, HIF1α and Runx2). Abrogating RANK or its downstream signaling network, c-Myc/Max or c-Met, abolished PCa skeletal metastasis in mice. We observed that a small number of RANKL-expressing PCa cells can initiate bone and soft tissue metastases by recruiting non-tumorigenic or bystander PCa or host cells from the circulation or at metastatic sites to co-colonize bone. The recruited bystander PCa cells assume the phenotypes of RANKL-expressing PCa cells by expressing increased c-Met, phosphorylated c-Met and RANKL. RANKL expression at a single cell level in primary PCa tissues predicted disease-specific survival, reflecting the significant role of RANKL-RANK signaling in the development of lethal bone metastasis. Global gene expression analysis perturbed by RANKL in LNRANKL compared to LNNeo cells.
2014-02-06 | E-GEOD-48432 | biostudies-arrayexpress
Project description:We found that RANKL, expressed by cancer cells or derived from exogenous sources, consistently induced human prostate, breast, kidney, lung and liver cancer cells to colonize or metastasize to bone in an animal model of cancer bone metastasis. RANK-mediated signaling established a premetastatic niche through a forward feedback loop by inducing RANKL and c-Met expression and downstream signaling via upregulation of master regulator transcription factors regulating EMT (Twist1, Slug, Zeb1, Zeb2), stem cells (Sox2, Myc, Oct3/4 and Nanog), neuroendocrine cells (Sox 9, HIF-1α and FoxA2) and osteomimicry (c-Myc/Max, Sox2, Sox9, HIF1α and Runx2). Abrogating RANK or its downstream signaling network, c-Myc/Max or c-Met, abolished PCa skeletal metastasis in mice. We observed that a small number of RANKL-expressing PCa cells can initiate bone and soft tissue metastases by recruiting non-tumorigenic or bystander PCa or host cells from the circulation or at metastatic sites to co-colonize bone. The recruited bystander PCa cells assume the phenotypes of RANKL-expressing PCa cells by expressing increased c-Met, phosphorylated c-Met and RANKL. RANKL expression at a single cell level in primary PCa tissues predicted disease-specific survival, reflecting the significant role of RANKL-RANK signaling in the development of lethal bone metastasis.
2014-02-06 | GSE48432 | GEO
Project description:Brain metastatic disease occurs in 10-30% of metastatic breast cancer cases. The incidence of brain metastases is increasing with median overall survival < 2 years for patients. In order to better characterize oncogenic pathway activity pertinent to breast cancer brain metastasis, exome capture RNA sequencing was carried out on patient matched primary breast with brain metastatic tumor samples for 45 cases of breast cancer brain metastasis (N= 90 samples). Here, exome capture RNA sequencing data is deposited as sequencing batch corrected log2 transformed trimmed M of means (TMM) normalized counts per million (CPM) (log2(TMM-CPM +1) gene expression values (n=16,714 protein coding genes; N=90 tumor samples).
2022-04-01 | GSE173661 | GEO
Project description:Brain metastatic disease occurs in 10-30% of metastatic breast cancer cases. The incidence of brain metastases is increasing with median overall survival < 2 years for patients. In order to better characterize oncogenic pathway activity pertinent to breast cancer brain metastasis, exome capture RNA sequencing was carried out on patient matched primary breast with brain metastatic tumor samples for 45 cases of breast cancer brain metastasis (N= 90 samples). Here, exome capture RNA sequencing data is deposited as sequencing batch corrected log2 transformed trimmed M of means (TMM) normalized counts per million (CPM) (log2(TMM-CPM +1) gene expression values (n=16,714 protein coding genes; N=90 tumor samples).
2021-11-12 | GSE184869 | GEO
Project description:Breast cancer is the leading type of cancer in women. Breast cancer brain metastasis is considered as an essential issue in breast cancer patients. Membrane proteins play important roles in breast cancer brain metastasis that contributes to the cell adhesion and penetration of blood-brain barrier. To achieve a deeper insight of the mechanism of breast cancer brain metastasis, liquid chromatography tandem mass spectrometry (LC-MS/MS) was performed to analyze the enriched membrane proteomes from six different breast cancer cell lines. Quantitative proteomic data of all cell lines were compared with MDA-MB-231BR which has the specific brain metastasis capacity. 1239 proteins were identified and 990 were quantified with more than 70% of membrane proteins in all cell lines. Each cell line can be separated apart from others in PCA. Ingenuity pathway analysis (IPA) supported the high brain metastatic ability of 231BR and suggested importance of the up-regulation of integrin proteins and down-regulation of EPHA in brain metastasis. 28 proteins were observed unique expression alteration in 231BR. The up-regulation of NPM1, hnRNP Q, hnRNP K and eIF3l and the down-regulation of TUBB4B and TUBB were observed to be associated with the brain metastasis cell line and may contributes to the breast cancer brain metastasis.
2017-05-23 | PXD005719 | Pride
Project description:Breast cancer brain metastasis
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Project description:Elevated Met receptor tyrosine kinase (RTK) expression correlates with poor outcome in breast cancer, yet a causal role for Met in the development of breast cancer has not been directly established. To examine this question, we generated a transgenic mouse model that targets expression of an oncogenic Met receptor (MetMut) to the mammary epithelium. We show that MetMut induces mammary tumors with a variety of histopathologies that exhibit gene expression profiles sharing similarities with human basal and luminal breast tumor subtypes. Among all breast cancers, we further demonstrate that the Met receptor is primarily overexpressed in human basal and HER2 positive breast cancers, and that a Met associated gene expression signature identifies patients with poor prognosis. Keywords: Met, mammary, poor outcome, EMT, basal breast cancer
2009-03-30 | GSE10450 | GEO
Project description:Triple-negative breast cancer (TNBC) is a heterogeneous disease that lacks both effective patient stratification strategies and therapeutic targets. In the present study, we assay tumour-initiating cells (TICs) properties, using established Met-dependent transgenic mouse models of TNBC, breast cancer cell lines and, patient-derived xenografts, to directly investigate the role of Met in tumour initiation and identify FGFR1 signaling as a key convergent pathway with Met for the maintenance of TICs. To understand the events that occur in TICs upon inhibition of Met and FGFR1, we performed gene expression profiling by RNA-Sequencing of RNA prepared from tumoursphere from 3 independent MMTV-Metmt;Trp53fl/+;Cre derived spindloid tumour cell lines (A1005, A1129, A1471) following treatment with Met or FGFR inhibitor alone (Crizotinib or PD173074, respectively), or in combination for 24h.
2020-11-28 | GSE162272 | GEO
Project description:MET exon 14 skipping alteration (MET∆14Ex) is an actionable oncogenic driver that occurs in 2-4% of non-small cell lung cancer (NSCLC) cases. However, the precise role of MET∆14Ex in tumor progression in NSCLC is poorly understood. We here demonstrate that MET∆14Ex expression increases receptor kinase activity and downstream signaling by impairing receptor internalization and endocytic degradation, which significantly boosts tumor cell scattering and invasion as well as metastasis. To explore the key mechanisms in regulation of these phenotypes, RNA sequencing (RNA-seq) studies were conducted on HGF-treated MET∆14Ex and MET cell models in an effort to identify the global change of transcriptome signature and key functional pathways involved in MET∆14Ex-medieated tumorigenesis. Both Ingenuity pathway analysis (IPA) and gene set enrichment analysis (GSEA) revealed an induction of a tight cluster of functional pathways associated with cell movement in HGF-treated MET∆14Ex models (vs MET) in a time-dependent manner.
2021-12-31 | GSE182684 | GEO