TGFB-responsive Human Trophoblast-derived Cell Lines

Placenta ◽  
2001 ◽  
Vol 22 (10) ◽  
pp. 889-890 ◽  
Author(s):  
P.K. Lala ◽  
C.G. Graham
Keyword(s):  
Stem Cells ◽  
2011 ◽  
pp. N/A-N/A ◽  
Author(s):  
Olga Genbacev ◽  
Matthew Donne ◽  
Mirhan Kapidzic ◽  
Matthew Gormley ◽  
Julie Lamb ◽  
...  

2019 ◽  
Vol 47 (3) ◽  
pp. 1319-1329 ◽  
Author(s):  
Jian Zhang ◽  
Hai Ma ◽  
Liu Yang ◽  
Hongchun Yang ◽  
Zhenxing He

Objectives Overexpression of human trophoblast cell surface antigen 2 (Trop2) has been observed in many cancers; however, its roles in proliferation, apoptosis, migration, and invasion of hepatocellular carcinoma (HCC) remain unclear. Thus, this study aimed to characterize the function of Trop2 in HCC. Methods Trop2 protein expression was detected by immunohistochemistry in HCC tissues. Cell proliferation, apoptosis, and invasion were respectively measured by CCK-8, flow cytometry, Transwell, and wound healing assays. Expression levels of epithelial–mesenchymal transition-related proteins and Trop2 protein in HCC cell lines were detected by western blotting after silencing of the TROP2 gene. Results Trop2 protein was highly expressed in HCC tissues and HCC cell lines. Trop2 mRNA and protein expression levels decreased in HepG2 and HCCLM3 cells after transfection with Trop2 siRNA. Silencing of the TROP2 gene in HepG2 and HCCLM3 cells strongly inhibited cell proliferation and migration, while enhancing cell apoptosis. Investigation of the molecular mechanism revealed that silencing of the TROP2 gene suppressed epithelial–mesenchymal transition of HepG2 and HCCLM3 cells. Conclusions The results of the present study may improve understanding of the role of Trop2 in regulation of cell proliferation and invasion, and may aid in development of novel therapy for HCC.


2006 ◽  
Vol 87 (7) ◽  
pp. 2067-2071 ◽  
Author(s):  
A. Muir ◽  
A. M. L. Lever ◽  
A. Moffett

The placenta is unique amongst normal tissues in transcribing numerous different human endogenous retroviruses at high levels. In this study, RT-PCR and immunohistochemistry were used to investigate the expression of syncytin in human trophoblast. Syncytin transcripts were found in first-trimester trophoblast cells with both villous and extravillous phenotypes and also in the JAR and JEG-3 choriocarcinoma cell lines. Syncytin protein was detected in villous trophoblast and in all extravillous trophoblast subpopulations of first- and second-trimester placental tissues. It was also present in ectopic trophoblast from tubal implantations. This study confirms that syncytin is expressed widely by a variety of normal human trophoblast populations, as well as choriocarcinoma cell lines.


2010 ◽  
Vol 16 (7) ◽  
pp. 481-491 ◽  
Author(s):  
C. Biondi ◽  
M. E. Ferretti ◽  
L. Lunghi ◽  
S. Medici ◽  
F. Cervellati ◽  
...  

2020 ◽  
Author(s):  
Jiawu Zhao ◽  
Rebecca P. Chow ◽  
Rebecca H. McLeese ◽  
Michelle B. Hookham ◽  
Timothy J. Lyons ◽  
...  

2020 ◽  
Author(s):  
Tadashi Sasagawa ◽  
Atsushi Jinno-Oue ◽  
Takeshi Nagamatsu ◽  
Kazuki Morita ◽  
Tetsushi Tsuruga ◽  
...  

Abstract Background: Soluble Fms-like tyrosine kinase-1 (sFLT1) as an anti-angiogenic factor is abundantly expressed in placental trophoblasts. Choriocarcinoma, a malignant tumor derived from trophoblasts, is known to be highly angiogenic and metastatic. However, the molecular mechanism underlying angiogenesis in choriocarcinoma pathogenesis remains unclear. We aimed to investigate the mRNA expression and DNA methylation status of the FLT1 gene in human choriocarcinoma cells and trophoblast cells. Methods: qRT-PCR, Western blotting and ELISA were conducted to evaluate the mRNA and protein expression levels of sFLT1. 5-aza-2'-deoxycytidine (5azadC) treatment and bisulfite sequencing were used to study the FLT1 gene promoter methylation. The effect of sFLT1 on choriocarcinoma growth and angiogenesis was evaluated in a xenograft mouse model. Results: Expression of the FLT1 gene was strongly suppressed in choriocarcinoma cell lines compared with that in the primary trophoblasts. Treatment of choriocarcinoma cell lines with 5azadC, a DNA methyltransferase inhibitor, markedly increased in mRNA expression of three FLT1 splice variants and secretion of sFLT1 proteins. Bisulfite sequencing revealed that the CpG hypermethylation was observed at the FLT1 promoter region in choriocarcinoma cell lines and a human primary choriocarcinoma tissue but not in human trophoblast cells. Interestingly, in 5azadC-treated choriocarcinoma cell lines, sFLT1 mRNA expression and sFLT1 production were further elevated by hypoxic stimulation. Finally, as expected, sFLT1-expressing choriocarcinoma cells implanted into nude mice showed significantly slower tumor growth and reduced microvessel formation compared with GFP-expressing control choriocarcinoma cells. Conclusions: Inhibition of sFLT1 production by FLT1 silencing occurs via the hypermethylation of its promoter in choriocarcinoma cells. The stable expression of sFLT1 in choriocarcinoma cells resulted in the suppression of tumor growth and tumor vascularization in vivo . We suggest that the FLT1 gene may be a cell-type-specific tumor suppressor in choriocarcinoma cells.


Placenta ◽  
2006 ◽  
Vol 27 (9-10) ◽  
pp. 934-938 ◽  
Author(s):  
E. Komiya ◽  
M. Kondoh ◽  
H. Mizuguchi ◽  
M. Fujii ◽  
N. Utoguchi ◽  
...  

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Mario Rothbauer ◽  
Nilaykumar Patel ◽  
Hajnalka Gondola ◽  
Monika Siwetz ◽  
Berthold Huppertz ◽  
...  

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