Gene profile in ovarian cancer cell spheroids
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE136924 | GEO | 2019/09/06
REPOSITORIES: GEO
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Project description:Cancer stem cells can self-renew, proliferate into differentiated cells, or enter a quiescent state and are regarded to cause chemoresistance and recurrence. Fresh tumor cells from three ovarian cancer patients were cultured to isolated spheroid-forming cells (SFC; cancer stem-like cells). The miRNAs that exhibited significant differential expression between SFCs and adherent cells were identified using miRNAs microarrays.
2019-09-06 | GSE136925 | GEO
Project description:GBM is the most common and aggressive primary brain tumor with dismal prognosis. NK cells are large granular lymphocytes with natural cytotoxicity against tumor cells, and they should be established for the novel treatment against patients with GBM. We have previously reported highly activated and ex vivo-expanded NK cells derived from human peripheral blood, which is designated as Genuine-induced natural killer cell (GiNK), induced by our specific culture conditions exerted the cytotoxic effect on GBM cells via apoptosis. First, we comprehensively summarized the molecular characteristics, especially focusing on the expression of stem cell markers, extracellular matrix markers, chemokine, chemokine receptors, and the NK receptors’ ligands, of GBM spheroids compared with 2D adherent GBM cells by using microarray. In the spheroid derived from GBM cell lines, gene expression of stem cell markers, extracellular matrix markers, chemokine, chemokine receptor, NK cell inhibitory receptor’ ligand were up-regulated compared with 2D adherent GBM cells. A preclinical evaluation of the NK cells was performed by ex vivo 3D spheroid model derived from GBM cell lines. In 3D spheroid model, the NK cells accumulated and infiltrated around the spheroids and induced the GBM cell death. Flow cytometry-based apoptosis detection assay clearly showed that the NK cells induced the GBM cell death via apoptosis. Our findings could provide pivotal information for the NK cell based-immunotherapy to patients with GBM.
2021-08-19 | GSE182373 | GEO
Project description:Epithelial ovarian cancer (EOC) is a high-risk cancer presenting with heterogeneous tumors. The high incidence of EOC metastasis from primary tumors to nearby tissues and organs is a major driver of EOC lethality. We used cellular models of spheroid formation and re-adherence to investigate cellular signaling dynamics in each step toward EOC metastasis. In our system, adherent cells model primary tumors, spheroids formation represents the initiation of metastatic spread, while re-adherent spheroid cells represent secondary tumors. Proteomic and phosphoproteomic analyses show that spheroid cells are hypoxic and show markers for cell cycle arrest. Aurora kinase B (AURKB) abundance and downstream substrate phosphorylation are significantly reduced in spheroids and re-adherent cells, explaining their cell cycle arrest phenotype. The proteome of re-adherent cells is most similar to spheroids, yet greater changes in the phosphoproteome show that spheroid cells stimulate Rho-associated kinase 1 (ROCK1) mediated signaling, which controls cytoskeletal organization. In spheroids, we found significant phosphorylation of ROCK1 substrates that were reduced in both adherent and re-adherent cells. Application of the ROCK1-specific inhibitor Y-27632 to spheroids increased the rate of re-adherence and spheroid density. The data suggest ROCK1 inhibition increases EOC metastatic potential. We identified novel pathways controlled by AURKB and ROCK1 as major drivers of metastatic behavior in EOC cells. Our data show that phosphoproteomic reprogramming precedes proteomic changes that characterize spheroid re-adherence in EOC metastasis.
2024-01-26 | PXD043220 | Pride
Project description:Purpose: To understand the changes in RNA expression in tumor-initiating cell (TIC) (spheroid) and non-TIC populations (adherent) in ovarian cancer. Methods: OV90 cells were grown in adherent (non-TIC) or spheroid (TIC) conditions. Total RNA was extracted from each condition and RNAseq was performed and analysed for differential gene expression between the conditions.
2020-10-03 | GSE158949 | GEO
Project description:GBM is the most common and aggressive primary brain tumor with dismal prognosis. NK cells are large granular lymphocytes with natural cytotoxicity against tumor cells, and they should be established for the novel treatment against patients with GBM. We have previously reported highly activated and ex vivo-expanded NK cells derived from human peripheral blood, which is designated as Genuine-induced natural killer cell (GiNK), induced by our specific culture conditions exerted the cytotoxic effect on GBM cells via apoptosis. First, we comprehensively summarized the molecular characteristics, especially focusing on the expression of stem cell markers, extracellular matrix markers, chemokine, chemokine receptors, and the NK receptors’ ligands, of GBM spheroids compared with 2D adherent GBM cells by using microarray. In the spheroid derived from GBM cell lines, gene expression of stem cell markers, extracellular matrix markers, chemokine, chemokine receptor, NK cell inhibitory receptor’ ligand were up-regulated compared with 2D adherent GBM cells. A preclinical evaluation of the NK cells was performed by ex vivo 3D spheroid model derived from GBM cell lines. In 3D spheroid model, the NK cells accumulated and infiltrated around the spheroids and induced the GBM cell death. Flow cytometry-based apoptosis detection assay clearly showed that the NK cells induced the GBM cell death via apoptosis. Our findings could provide pivotal information for the NK cell based-immunotherapy to patients with GBM.
2021-08-19 | GSE182374 | GEO
Project description:During tumor progression, cancer cells rewire their metabolism to face their bioenergetic demands. In recent years, microRNAs (miRNAs) have emerged as regulatory elements that inhibit the translation and stability of crucial mRNAs, some of them causing direct metabolic alterations in cancer. In this study, we investigated the relationship between miRNAs and their targets mRNAs that control metabolism, and how this fine-tuned regulation is diversified depending on the tumor stage. To do so, we implemented a paired analysis of RNA-seq and small RNA-seq in a breast cancer cell line (MCF7). The cell line was cultured in multicellular tumor spheroid (MCTS) and monoculture conditions. For MCTS, we selected two-time points during their development to recapitulate a proliferative and quiescent stage and contrast their miRNA and mRNA expression patterns associated with metabolism. As a result, we identified a set of new direct putative regulatory interactions between miRNAs and metabolic mRNAs representative for proliferative and quiescent stages. Notably, our study allows us to suggest that miR-3143 regulates the carbon metabolism by targeting hexokinase-2. Also, we found that the overexpression of several miRNAs could directly overturn the expression of mRNAs that control glycerophospholipid and N-Glycan metabolism. While this set of miRNAs downregulates their expression in the quiescent stage, the same set is upregulated in proliferative stages. This last finding suggests an additional metabolic switch of the above mentioned metabolic pathways between the quiescent and proliferative stages. Our results contribute to a better understanding of how miRNAs modulate the metabolic landscape in breast cancer MCTS, which eventually will help to design new strategies to mitigate cancer phenotype.
2020-11-11 | E-MTAB-9741 | biostudies-arrayexpress
Project description:Anchorage-independent spheroid cells of HCC possess stemness properties. Huh7 cells are cultured in ultra-low attachment surface plates with serum-free medium. RNA-sequencing (RNA-seq) was applied in spheroid culture cells and adherent culture cells.
2022-06-01 | GSE199940 | GEO
Project description:Spheroid cells derived from colon cancer patients was treated with Y-27632, a ROCK inhibitor, and we have performed whole genome microarray expression assay.
2021-04-01 | GSE117505 | GEO
Project description:Cell-based approaches utilizing autologous human renal cells require their isolation, expansion in vitro and reintroduction back into the host for renal tissue regeneration. Nevertheless, human kidney epithelial cells (hKEpC) lose their phenotype, dedifferentiate and assume the appearance of fibroblasts after relatively few passages in culture. We hypothesized that growth conditions may influence hKEpC phenotype and function. hKEpC retrieved from human nephrectomy tissue samples showed the ability to reproducibly form kidney-spheres when grown in suspension culture developed in non-adherent conditions. Genetic labeling and time-lapse microscopy indicated, at least in part, the aggregation of hKEpC into 3D-spheroids rather than formation of pure clonally expanded spheres. Characterization of hKEpC spheroids by real-time PCR and FACS analysis showed up-regulation of some renal developmental and 'stemness' markers compared to monolayer and mostly an EpCAM+CD24+CD133+CD44+ spheroid cell phenotype. Oligonucleotide microarrays which were used to identify global transcriptional changes accompanying spheroid formation, showed predominantly up-regulation of cell matrix/cell contact molecules and cellular biogenesis processes and down-regulation of cell cycle, growth and locomotion. Accordingly, hKEpC spheroids proliferated slowly as indicated by low Ki-67 staining, but when grafted in low cell numbers onto the chorioallantoic membrane (CAM) of the chick embryo, they exclusively reconstituted various renal tubular epithelia. Moreover, efficient generation of kidney spheroids was observed after long-term monolayer culture resulting in re-establishment of tubulogenic capacity upon CAM grafting. Thus, generation of a specialized quiescent niche in hKEpC spheroids may provide a functional benefit for kidney-derived cells in vivo. 6 samples, 3 adherent and 3 spheroids samples
2011-12-31 | E-GEOD-28052 | biostudies-arrayexpress
Project description:Colorectal cancers have a rare population of cells that express specific cell surface markers, and are referred to as cancer stem cells (CSC). Targeting CSCs, implicated in tumor relapse, is a paradigm shifting approach for colorectal cancer. We used gene microarray to analyze gene expression in HT-29, a colon cancer cell line, grown as monolayer and spheroid and identify metabolic pathways that are upregulated.
2015-04-01 | GSE65433 | GEO