Rituximab, a monoclonal antibody against CD20, has achieved great success in the treatment of B cell lymphoma, but many patients have shown resistance to it and led to disease progression eventually. At present, the mechanism of resistance is still not clear, but we consider that it may involve the multiple genes and multiple signaling pathways. Therefore, our study aimed at searching differentially expressed genes of rituximab resistant cell lines (RRCL) by cDNA microarray, and exploring the resistant mechanism of RRCL by using the subsequent bioinformatics methods. In this study, we successfully identified seventy up-regulated genes and forty-two down-regulated genes in both two RRCL. We also isolated the MAPK signaling pathway, which was the significantly enriched pathway in resistant mechanism, through KEGG pathway analysis. Moreover, we discovered the biological behaviors of RRCL that mainly inhibit apoptosis, promote cellular proliferation, transcription and angiogenesis through Gene Ontology (GO) terms analysis. In conclusion, our results suggested that the most closely related pathway to rituximab resistance was MAPK signaling pathway, which may partly be related to its inhibiting the apoptosis of cells and promoting the proliferation of cells and vascular development.
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Specimen part, Cell line
View SamplesCompare with normal nasopharyngeal epithelial cells, we found BDH2 was decreased in NPC cells, we found that BDH2 inhibited proliferation, colony formation, migration and invasion in NPC cells.
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Specimen part, Cell line
View SamplesCompare with normal nasopharyngeal epithelial cells, we found ACAT1 was decreased in NPC cells, we found that ACAT1 inhibited proliferation, colony formation, migration and invasion in NPC cells. We used microarrays to identify differential genes regulated by ACAT1 in NPC cell lines.
Epigenetic Inactivation of Acetyl-CoA Acetyltransferase 1 Promotes the Proliferation and Metastasis in Nasopharyngeal Carcinoma by Blocking Ketogenesis.
Cell line, Treatment
View SamplesLatent infection with Epstein-Barr virus (EBV) is recognised as a factor in the pathogenesis of nasopharyngeal carcinoma (NPC). We found that EBV encoded Latent membrane protein 2A (LMP2A) enhances lipid accumulation significantly in NPC cells.
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Sex, Specimen part, Cell line
View SamplesTumor progression is associated with an immunosuppressive microenvironment that consists of several elements, such as regulatory T cells, type 2 macrophages and myeloid-derived suppressor cells. Here, we identify for the first time a BDCA1+CD14+ population of immunosuppressive cells that resides both in the blood and tumor of melanoma patients. We demonstrated that the presence of these cells in dendritic cell (DC)-based anti-tumor vaccines significantly suppresses CD4+ T cells in an antigen-specific manner. In an attempt to reveal the mechanism of this suppressive activity, we noticed that BDCA1+CD14+ cells express elevated levels of the check-point molecule PD-L1, which thereby hinders T cell proliferation. Importantly, although this suppressive BDCA1+CD14+ population expresses markers of both BDCA1+ DCs and monocytes, functional, transcriptome and proteome analyses clearly revealed that they comprise a unique population of cells that is exploited by tumors to evade immunity. Thus, targeting these cells may improve the efficacy of cancer immunotherapy.
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View SamplesTo induce a differentiated phenotype, primary pancreatic TIC cultures were grown in 10% FBS containing conditions. To analyze gene expression changes upon induction of a differentiated phenotype, total RNA of cells cultured in FBS containing conditions and parallel control cells cultured under serum-free conditions was isolated and comparative gene expression profiling was performed.
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No sample metadata fields
View SamplesMouse gene express was using Mouse Gene 1.0 ST Array.
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Specimen part
View SamplesTo study the drug resistant phenotype between stem-like cancer cells at different EMT status, we isolated 4 subpopulations from the non-small-cell lung cancer cell line (PC14) according to the E-cadherin and CD133 expression level. We demonstrated that the epithelial type CD133high stem-like cells (E-cadhighCD133high) significantly exhibited higher drug resistant ability compared to the mesenchymal type CD133high stem-like cells (E-cadlowCD133high), epithelial type CD133low non-stem like cells (E-cadhighCD133low) and mesenchymal type CD133low non-stem like cells (E-cadlowCD133low).
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Cell line
View SamplesActive HUMSC with distinct binding rate to MDA MB-231 breast cancer cells, distinct ability in suppressing tumorigenesis,distinct cell in cell features and distinct features under TEM then inactive HUMSC
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Specimen part
View SampleshUC-MSCs exhibit the biological characteristics and potential for neural differentiation.The different gene involved in the neural differentiation were not clear.
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Specimen part
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