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Gene expression of human cancer cells co-cultured with mouse astrocytes and fibroblasts after series of cross co-culture

ABSTRACT: Brain metastases are highly resistant to chemotherapy. Brain metastases are surrounded and infiltrated by activated astrocytes. To examine the genes whose expression is associated with chemo-resistance of brain-metastasized cancer cells, gene expression data were collected and analyzed from breast cancer cells and lung cancer cells co-cultured with astrocytes. Fibroblast cells were used as control.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26292 | GEO | 2012/12/31

SECONDARY ACCESSION(S): PRJNA142309

REPOSITORIES: GEO

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Gene expression of human cancer cells co-cultured with mouse astrocytes and fibroblasts after series of cross co-culture

Project description:Brain metastases are highly resistant to chemotherapy. Brain metastases are surrounded and infiltrated by activated astrocytes. To examine the genes whose expression is associated with chemo-resistance of brain-metastasized cancer cells, gene expression data were collected and analyzed from breast cancer cells and lung cancer cells co-cultured with astrocytes. Fibroblast cells were used as control. Human lung cancer cell PC14 was co-cultured with mouse astrocytes or fibroblasts for two rounds. Total RNAs were extracted from co-cultured cells and hybridized to human microarray.

2012-12-31 | E-GEOD-26292 | biostudies-arrayexpress

Cross species hybridization of human cancer cells co-cultured with mouse astrocytes and fibroblasts (Illumina human-6)

2012-12-31 | GSE26291 | GEO

Cross species hybridization of human cancer cells co-cultured with mouse astrocytes and fibroblasts (Illumina mouse-6)

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Cross species hybridization of human cancer cells co-cultured with mouse astrocytes and fibroblasts (Illumina mouse-6)

Project description:Brain metastases are highly resistant to chemotherapy. Brain metastases are surrounded and infiltrated by activated astrocytes. To examine the genes whose expression is associated with chemo-resistance of brain-metastasized cancer cells, gene expression data were collected and analyzed from breast cancer cells and lung cancer cells co-cultured with astrocytes. Fibroblast cells were used as control. Total RNAs were extracted from co-cultured cells and hybridized to human microarray and mouse microarrays to detect human cell and mouse cell specific gene expression data.

2012-12-31 | E-GEOD-26261 | biostudies-arrayexpress

Cross species hybridization of human cancer cells co-cultured with mouse astrocytes and fibroblasts (Illumina human-6)

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2012-12-31 | E-GEOD-26291 | biostudies-arrayexpress

SKBR3/HER2+ Breast Cancer Cellular Response to Brain Cell-Secreted Factors

Project description:To address the challenges associated with the investigation of brain-metastasized cancers and provide insights into the drivers of cancer cell behavior at the brain metastatic site, this study was aimed at exploring the response of SKBR3/HER2+ cells to neural factors secreted by brain cells that come first in contact with the metastasized cancer cells, i.e., human endothelial cells (HBEC5i), astrocytes (NHA), and microglia (HMC3). To this end, serum-starved breast cancer cells were exposed to the combined secretome of brain cells, allowed to grow for 24h, and analyzed by LC-MS/MS using an Orbitrap QE instrument to generate and compare the whole cell proteome profiles of treated vs non-treated cells.

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Intercellular transfer of small RNAs from astrocytes to lung tumor cells induces resistance to chemotherapy.

Project description:Brain metastases are highly resistance to chemotherapy and have a poor prognosis for cure. Tumor cells are surrounded by activated astrocytes and exploit their cyto-protective properties for protection from apoptosis induced by chemotherapy. The mechanism by which astrocytes protect tumor cells is poorly understood. An important non-mutational mechanism of chemotherapy resistance is regulation of gene translation mediated by small non-coding RNAs (sRNAs), in particular, microRNAs (miRNAs). Here we studied the role of astrocytic sRNAs in promoting resistance of the human lung tumor PC14 cells to apoptosis induced by chemotherapy. To this end we compared the sRNA profile of human lung tumor cells that were cultured with or without astrocytes by miRNA microarray. The results show that sRNAs are transferred from astrocytes to PC14 cells in a contact-dependent manner. This transfer is fast and reached plateau already after six hours of co-culturing. Carbenoxolone, a broad-spectrum gap junction antagonist, inhibited the sRNAs transfer indicating that the sRNAs are transferred via gap-junction, maybe via survival pathways. Enforced expression of these sRNA in PC14 cells increased their resistance to the chemotherapy agent Taxol. In light of these results, we offer novel findings that may be clinically relevant to treatment development for brain metastases.

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Project description:Immunotherapies against brain metastases have shown clinical benefits mainly when applied to locally asymptomatic patients. It is currently unclear why responses to this therapy drop in symptomatic brain metastases, since the use of corticoids is not consistently involved. We report here that a subpopulation within STAT3+ brain metastasis-associated astrocytes is responsible to block the anti-tumor activity of infiltrating CD8+ T cells. The underlying molecular crosstalk involving astrocyte-secreted TIMP1 signaling on CD63+ CD8+ T cells proves a strong immunomodulatory role of astrocytes in the context of brain metastases. By using genetic and pharmacologic approaches applied not only to mouse models, but also to alive human brain metastases we conclude that a combined immunotherapy blocking this local immunosuppressive hub could benefit patients with symptomatic brain metastases. Furthermore, the detection of TIMP1 in the CSF provides a biomarker to select patients for this therapeutic approach. Our findings uncover the importance of dissecting the heterogeneity within the microenvironment at the functional level and the emerging cellular networks to improve the efficacy of organ-specific therapies in metastasis.

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Type I Interferon Response in Astrocytes Promotes Brain Metastasis by Enhancing Monocytic Myeloid Cell Recruitment

Project description:Cancer metastasis to the brain is a significant clinical problem. Metastasis is the consequence of favorable interactions between invaded cancer cells and the microenvironment. Here, we demonstrate that cancer-activated astrocytes create a sustained low-level activated type I interferon (IFN) microenvironment in brain metastatic lesions. We further confirm that the IFN response in astrocytes facilitate brain metastasis. Mechanistically, IFN signaling in astrocytes activates C-C Motif Chemokine Ligand 2 (CCL2) production, which further increases the recruitment of monocytic myeloid cells. The correlation between CCL2 and monocytic myeloid cells is confirmed in clinical brain metastasis samples. Lastly, genetically or pharmacologically inhibiting C-C Motif Chemokine Receptor 2 (CCR2) significantly reduces brain metastases. Our study clarifies a pro-metastatic effect of type I IFN in the brain even though IFN response has been considered to have anti-tumor effects. Moreover, this work expands our understandings on the interactions between cancer-activated astrocytes and immune cells in brain metastasis.

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An ecosystem mimicking brain development promotes metastatic growth of SCLC in the brain

Project description:Small cell lung cancer (SCLC) is a fatal form of cancer that frequently metastasizes to the brain. Here we investigated the mechanisms allowing SCLC cells to grow in the unique brain microenvironment. We found that neuronal programs upregulated in SCLC cells during tumor progression and upon growth in the brain are critical for SCLC growth in the brain. Mechanistically, the presence of SCLC cells in the brain re-activates astrocytes, which in turn promote the survival of SCLC cells by secreting neuronal pro-survival factors such as SERPINE1. We also identified Reelin, a molecule produced by developing neurons to recruit astrocytes, as a molecule secreted by SCLC cells to recruit astrocytes to the tumor site and promote SCLC growth in the brain. Thus, SCLC cells co-opt mechanisms normally at play between astrocytes and neurons to promote SCLC growth in the brain. Targeting such developmental neuronal programs may help treat brain metastases.

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