Cytogenetic and DNA-fingerprint characterization of choriocarcinoma cell lines and a trophoblast/choriocarcinoma cell hybrid.
ABSTRACT We report the successful fusion of human choriocarcinoma cells with normal human trophoblast cells to a choriocarcinoma/trophoblast hybrid. The hybrid cells ACH1P were derived from fusion of primary male trophoblast cells with the HGPRT-defective choriocarcinoma cell line AC1-1. The karyotypes of the parental choriocarcinoma cell line JEG-3, its HGPRT-defective mutant clones AC1-1, AC1-5, and AC1-9, and the choriocarcinoma/trophoblast hybrid ACH1P are presented, together with a detailed characterization of the AC1-specific chromosomal marker add(X)(q26) using conventional cytogenetic banding techniques and multiplex-fluorescence in situ hybridization (M-FISH). To our knowledge, this is the first report of a stably proliferating human cell hybrid of trophoblastic origin, providing a unique cell culture model to study trophoblast-related invasion and its underlying genetic mechanisms.
- Journal of The American College of Cardiology - J AMER COLL CARDIOL. 01/2011; 57(14).
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ABSTRACT: The ubiquitously expressed serine/threonine specific casein kinase 1 (CK1) family plays important roles in the regulation of various physiological processes. Small-molecule inhibitors, such as the CK1δ/ε selectively inhibitor IC261, have been used to antagonize CK1 phosphorylation events in cells in many studies. Here we present data to show that, similarly to the microtubule destabilizing agent nocodazole, IC261 depolymerizes microtubules in interphase cells. IC261 treatment of interphase cells affects the morphology of the TGN and Golgi apparatus as well as the localization of CK1δ, which co-localizes with COPI positive membranes. IC261-induced depolymerization of microtubules is rapid, reversible and can be antagonized by pre-treatment of cells with taxol. At lower concentrations of IC261, mitotic spindle microtubule dynamics are affected; this leads to cell cycle arrest and, depending on the cellular background, to apoptosis in a dose-dependent manner. In addition, FACS analysis revealed that IC261 could induce apoptosis independent of cell cycle arrest. In summary this study provides additional and valuable information about various IC261-induced effects that could be caused by microtubule depolymerization rather than by inhibition of CK1. Data from studies that have used IC261 as an inhibitor of CK1 should be interpreted in light of these observations.PLoS ONE 01/2014; 9(6):e100090. · 3.73 Impact Factor
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ABSTRACT: The differential reaction of cytotrophoblast and syncytiotrophoblast towards infection with listeria monocytogenes (LM) is pivotal to its pathogenicity. In this study we tested the cytokine signature upon infection with listeria monocytogenes (LM) in an in vitro model. We compared two related trophoblastic cell lines (AC-1M32 and ACH1P). The cell line ACH1P showed syncytium formation, whereas AC-1M32 did not fuse, as demonstrated with immunfluorescence E-Cadherin staining. In a Multi-Analyte ELISArray we tested for concentrations of TNFα, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, IL-17A, IL-8, MCP1, MIP-1a, MIP-1b, MDC, Eotaxin, IFNγ, G-CSF, TGFβ1 after 8 and 24 hours. Compared to unstimulated cells, the syncytial cell line ACH1P showed a significant induction of Interleukin-6 (IL-6), Monocyte Chemotactic Protein-1 (MCP-1) and transforming growth factor β-1 (TGFβ1). Incubating AC-1M32 with LM, however, showed significantly reduced IL-6 levels and a massively increased (~300fold) TGFβ1 secretion compared to unstimulated controls. A functional anti-LM immune response was only induced by the syncytium-forming cell line ACH1P. Using the two sister cell lines AC-1M32 and ACH1P in an in vitro LM-stimulation assay might facilitate research in the area of placental listeria infection.American Journal Of Reproductive Immunology 08/2012; 68(5):387-91. · 3.32 Impact Factor