Single-cell cloning of cancer cells secreting specific subsets of extracellular vesicles
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ABSTRACT:
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE179115 | GEO | 2021/09/15
REPOSITORIES: GEO
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Project description:Extracellular vesicles (EVs) mediate communication in health and disease. Conventional assays are limited in profiling EVs secreted from large populations of cells and cannot map EV secretion onto individual cells and their functional profiles. We developed a high-throughput single-cell technique that enabled the mapping of dynamics of EV secretion. By utilizing breast cancer cell lines, we established that EV secretion is heterogeneous at the single-cell level and that non-metastatic cancer cells can secrete specific subsets of EVs. Single-cell RNA sequencing confirmed that pathways related to EV secretion were enriched in the non-metastatic cells compared with metastatic cells. We established isogenic clonal cell lines from non-metastatic cells with differing propensities for CD81+CD63+EV secretion and showed for the first time that specificity in EV secretion is an inheritable property preserved during cell division. Combined in vitro and animal studies with these cell lines suggested that CD81+CD63+EV secretion can impede tumor formation. In human non-metastatic breast tumors, tumors enriched in signatures of CD81+CD63+EV have a better prognosis, higher immune cytolytic activity, and enrichment of pro-inflammatory macrophages compared with tumors with low CD81+CD63+EVs signatures. Our single-cell methodology enables the direct integration of EV secretion with multiple cellular functions and enables new insights into cell/disease biology.
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Project description:Single-cell cloning of cancer cells secreting specific subsets of extracellular vesicles
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Project description:Breast tumour cells were found to remodel the bone marrow vascular microenviornment to support metastatic expansion. To identify tumour-derived factors that stimulate marrow endothelium, we studied the transcriptomes of four isogenic murine mammary tumour cell lines, 4T1.2, 4T1, 66cl4 and 67NR.
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Project description:Epithelial-mesenchymal transition (EMT) has been linked to cancer progression and metastatic propensity. The 4T1 tumor is a clinically relevant model of spontaneous breast cancer metastasis. Here we characterize 4T1-derived cell lines for EMT, in vitro invasiveness and in vivo metastatic ability. Contrary to expectations, the 67NR cells, which form primary tumors but fail to metastasize, express vimentin and N-cadherin, but not E-cadherin. 4T1 cells, however, express E-cadherin, are highly migratory and invasive, and metastasize to multiple sites. The 66cl4 metastatic cells display mixed epithelial and mesenchymal markers, but are less migratory and invasive than 67NR cells. These findings demonstrate that the metastatic ability of breast cancer cells does not correlate with genotypic and phenotypic properties of EMT per se, and suggest that other processes may govern metastatic capability. Gene expression analysis also has not identified differences in EMT markers, but has identified several candidate genes that may influence metastatic ability. Experiment Overall Design: Female BALB/c mice were injected with 1x10^6 viable cells (3 mice with 4T1/CMVLUC, 3 mice with 66cl4/CMVLUC, and 3 mice with 67NR/CMVLUC) into the right fourth mammary gland. 15 days after injection primary tumors were excised, and total RNA for microarray hybridization was isolated from the tumor part of laser capture microdissected sections.
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Project description:We aimed to identify metastatic disease prior to the formation of an overt secondary tumor in triple-negative breast cancer using sister cell lines 4T1 (metastatic), 4T07 (invasive, non-metastatic), and 67NR (non-metastatic). We used a porous, polycaprolactone scaffold, that serves as an engineered metastatic niche, to identify metastatic disease through the changing microenvironment.
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Project description:Epithelial-mesenchymal transition (EMT) has been linked to cancer progression and metastatic propensity. The 4T1 tumor is a clinically relevant model of spontaneous breast cancer metastasis. Here we characterize 4T1-derived cell lines for EMT, in vitro invasiveness and in vivo metastatic ability. Contrary to expectations, the 67NR cells, which form primary tumors but fail to metastasize, express vimentin and N-cadherin, but not E-cadherin. 4T1 cells, however, express E-cadherin, are highly migratory and invasive, and metastasize to multiple sites. The 66cl4 metastatic cells display mixed epithelial and mesenchymal markers, but are less migratory and invasive than 67NR cells. These findings demonstrate that the metastatic ability of breast cancer cells does not correlate with genotypic and phenotypic properties of EMT per se, and suggest that other processes may govern metastatic capability. Gene expression analysis also has not identified differences in EMT markers, but has identified several candidate genes that may influence metastatic ability. Keywords: cell type comparison
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2014-09-05 | E-GEOD-53124 | biostudies-arrayexpress
Project description:Glioblastoma cells are characterized by a highly invasive behavior whose mechanisms are not yet understood. Using the wound healing and Boyden chamber assays we compared in the present study the migration and invasion abilities of 5 glioblastoma cell lines (DK-MG, GaMG, U87-MG, U373-MG, SNB19) differing in p53 and PTEN status. We also analyzed by Western blotting the expression of PTEN, p53, mTOR and several other marker proteins involved in cell adhesion, migration and invasion. Among 5 cell lines, GaMG cells exhibited the fastest rate of wound closure, whereas U87-MG cells showed the most rapid chemotactic migration in the Boyden chamber assay. In DK-MG and GaMG cells, F-actin mainly occurred in the numerous stress fibers spanning the cytoplasm, whereas U87-MG, U373-MG and SNB19 cells preferentially expressed F-actin in filopodia and lamellipodia. Moreover, the two glioblastoma lines mutated in both p53 and PTEN genes (U373-MG and SNB19) were found to exhibit the fastest invasion rates through the Matrigel matrix.
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Project description:The long noncoding RNA LINC00152 shows ubiquitous expression and is often upregulated in tumor entities compared to healthy tissues. LINC00152 promotes malignant progression in the glioblastoma cell line U87. Here, LINC00152 knockdown leads to a reduction of migration and invasion of tumor cells. However, LINC00152 seems to have an opposite effect in another glioblastoma cell line A172. For this reason, the transcriptional patterns after LINC00152 knockdown in both cell lines (U87 and A172) were compared to identify the differences.
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