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Expression data generated by full-length and truncated syndecan-1 overexpression in B6FS fibrosarcoma cell line

ABSTRACT: To dissect the functions of syndecan-1 in the nucleus, and separate them from functions related to the cell-surface, we transfected fibrosarcoma cells with two constructs: one encoding the full-length syndecan-1, which translocates to the nucleus and another encoding syndecan-1 lacking the RMKKK nuclear localization signal with hampered nuclear translocation. Using this model system, we combined global transcriptomic and proteomic approaches in order to disclose the molecular mechanisms governing the nuclear translocation and its related functions. Our analysis identified several genes and pathways related to the nuclear compartment TGF-β pathway was activated by nuclear syndecan-1 and three genes were significantly altered by NLS deletion: NEK11 , DOCK8 , and EGR-1 as potential candidates coupled to syndecan-1 in the nucleus.

ORGANISM(S): Homo sapiens

PROVIDER: GSE81504 | GEO | 2017/09/10

SECONDARY ACCESSION(S): PRJNA321830

REPOSITORIES: GEO

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Project description:We aimed to investigate the function of syndecan-1 in tumor cell adhesion and migration, with special focus on the importance of its distinct protein domains, to better understand the structure-function relationship of syndecan-1 in tumor progression. We utilized two mesenchymal tumor cell lines which were transfected to stably overexpress full-length syndecan-1 or truncated variants: the 78 which lacks the extracellular domain except the DRKE sequence proposed to be essential for oligomerization, the 77 which lacks the whole extracellular domain, and the RMKKK which serves as a nuclear localization signal. Various bioassays for cell adhesion, chemotaxis, random movement and wound healing were studied. Furthermore we performed gene microarray to analyze the global gene expression pattern influenced by syndecan-1. We found that full-length syndecan-1 enhanced cell adhesion in a dose-dependent manner. The truncated constructs only affected adhesion marginally, or not at all. Both full-length syndecan-1 and all its distinct domains inhibited serum-induced cell migration and wound closure. The full-length syndecan-1 and the 78 constructs specifically reduced cell motility/migration in random movement assay. Cell adhesion depends on the extracellular domain and also associates with the DRKE motif. Effects of syndecan-1 on migration are more complex; the pro-adhesive effect of the extracellular domain is one factor hampering migration, but the transmembrane/cytoplasmic portion seems to have additional impact. Gene microarray analysis showed that a number of genes involved in cell adhesion and migration were differentially expressed in syndecan-1 overexpressing cells. Our results demonstrate that syndecan-1 regulates mesenchymal tumor cell adhesion and migration, and different domains have differential effects. Our study provides new inputs into the better understanding of structure-function relationship of this PG in tumor progression. Gene expression profiles (Human Gene 1.0 ST) of malignant mesothelioma cells were studied in syndecan-1 overexpressing cells (N=3) and vector control cells (N=3) .

Project description:Tomida2003 - NFAT functions Calcium Oscillation This model is described in the article: NFAT functions as a working memory of Ca2+ signals in decoding Ca2+ oscillation. Tomida T, Hirose K, Takizawa A, Shibasaki F, Iino M. EMBO J. 2003 Aug; 22(15): 3825-3832 Abstract: Transcription by the nuclear factor of activated T cells (NFAT) is regulated by the frequency of Ca(2+) oscillation. However, why and how Ca(2+) oscillation regulates NFAT activity remain elusive. NFAT is dephosphorylated by Ca(2+)-dependent phosphatase calcineurin and translocates from the cytoplasm to the nucleus to initiate transcription. We analyzed the kinetics of dephosphorylation and translocation of NFAT. We show that Ca(2+)-dependent dephosphorylation proceeds rapidly, while the rephosphorylation and nuclear transport of NFAT proceed slowly. Therefore, after brief Ca(2+) stimulation, dephosphorylated NFAT has a lifetime of several minutes in the cytoplasm. Thus, Ca(2+) oscillation induces a build-up of dephosphorylated NFAT in the cytoplasm, allowing effective nuclear translocation, provided that the oscillation interval is shorter than the lifetime of dephosphorylated NFAT. We also show that Ca(2+) oscillation is more cost-effective in inducing the translocation of NFAT than continuous Ca(2+) signaling. Thus, the lifetime of dephosphorylated NFAT functions as a working memory of Ca(2+) signals and enables the control of NFAT nuclear translocation by the frequency of Ca(2+) oscillation at a reduced cost of Ca(2+) signaling. This model is hosted on BioModels Database and identified by: BIOMD0000000678. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Expression data generated by full-length and truncated syndecan-1 overexpression in B6FS fibrosarcoma cell line

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