Cytogenetic and DNA-Fingerprint Characterization of Choriocarcinoma Cell Lines and a Trophoblast /Choriocarcinoma Cell Hybrid

RWTH Aachen University, Aachen, North Rhine-Westphalia, Germany
Cancer Genetics and Cytogenetics (Impact Factor: 1.93). 01/2000; 116(1):16-22. DOI: 10.1016/S0165-4608(99)00107-7
Source: PubMed


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.

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    • "For in cell culture experiments the following cell lines were used: Normal rat kidney cells (NRK) [51], immortalized rat fibroblast cells (F111) [52], NRK cells stably expressing GFP-TGN38 (Kplus) [53], Cercopithecus aethiops monkey kidneys cells (CV-1) [54] and CV-1 cells stably expressing EYFP-tubulin (see below) which were grown in DMEM. Furthermore we used the human cell line AC1-M88 generated by fusion of extravillous trophoblasts with a choriocarcinoma cell line [55], [56] that was cultured in DMEM/F-12 medium (both Gibco). Media were supplemented with 10% fetal calf serum (FCS; Biochrom) and cells were grown at 37°C in a humidified 5% CO2 atmosphere. "
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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 06/2014; 9(6):e100090. DOI:10.1371/journal.pone.0100090 · 3.23 Impact Factor
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    • "We tried to identify the protein responsible for this reactivity. Cell extracts were prepared from a choriocarcinoma–trophoblast hybrid cell line, AC-1M32 (Frank et al. 2000; deposited and available at the DSMZ,, #ACC442), used as a model for trophoblast. "
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    ABSTRACT: CD133 is an antigen expressed on hematopoietic progenitor cells and on some epithelial cells. We previously reported that a commercially available antibody against CD133, CD133-2/AC141, also reacted with an intracellular protein in placental trophoblasts. Here we show by 2D electrophoresis and mass spectroscopy that this reactivity is with cytokeratin 18, a cytokeratin present in most simple epithelia. Immunohistochemistry (IHC) with CD133-2/AC141 on a trophoblast cell line displayed a staining pattern typical for the cytoskeleton. Cryostat sections of stratified epithelia lacking cytokeratin 18 did not react with CD133-2/AC141. In conclusion, care must be taken not to misinterpret staining patterns using CD133-2/AC141 in IHC.
    Journal of Histochemistry and Cytochemistry 09/2002; 50(8):1131-4. DOI:10.1177/002215540205000814 · 1.96 Impact Factor
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    • "sons. For the analysis of neoplastic trophoblast, nude mice (Han:NMRI nu/nu) were injected subcutaneously with 10 6 AC-1M81 human choriocarcinoma/trophoblast hybrid cells (Frank et al., 1999) suspended in 0.2 ml volume. Human placental samples and tumors were fixed for a maximum of 24 hr in neutrally buffered 4% formaldehyde . "
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    ABSTRACT: In the mouse fetus, Mest is widely expressed in mesoderm derived tissues. In separate studies in mice and in humans, it has been shown to be maternally imprinted, that is, only the paternally inherited allele is active. Here, we show that starting with implantation, Mest is also expressed in maternal decidua of the mouse and in placenta of both humans and mice. Expression in murine decidua was restricted to endothelial cells. After Day 7, expression in the decidua gradually decreased. Mest-specific RT-PCR and restriction fragment length variant (RFLV) analysis of decidualized endometrium isolated from (M. musculus × M. spretus)F1 females showed that only the paternally derived Mest allele was activated in the decidual endothelium. In the mouse extraembryonic tissues, Mest transcripts were detected in derivatives of extraembryonic mesoderm only. Here, hemangioblast precursor cells and endothelial cells were positive. At all developmental stages of the mouse, trophoblast-derived cells were clearly devoid of Mest transcripts. In the human placenta MEST transcripts were also detected in hemangioblast precursor cells, however, MEST was also expressed in villous and invasive cytotrophoblast. In a human choriocarcinoma/trophoblastic tumour grown in a nude mouse, human MEST was expressed in the tumour cells, whereas murine Mest was expressed in endothelia of the murine capillaries. The expression pattern exhibited by both Mest and MEST in extraembryonic tissues during development and during formation of choriocarcinoma/trophoblast tumour suggests a functional role of the MEST proteins related to oncofetal angiogenesis. Dev Dyn 2000;217:1–10. ©2000 Wiley-Liss, Inc.
    Developmental Dynamics 02/2000; 217(1):1 - 10. DOI:10.1002/(SICI)1097-0177(200001)217:1<1::AID-DVDY1>3.0.CO;2-4 · 2.38 Impact Factor
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