2005
DOI: 10.3892/ijo.26.5.1193
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Differential expression and cytoplasm/membrane distribution of endoglin (CD105) in human tumour cell lines: Implications in the modulation of cell proliferation

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Cited by 24 publications
(25 citation statements)
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“…Comparative analysis of the CD105 (endoglin) receptor expression of different human tumor cells indicated two protein pools, one of which accounted for receptor surface expression, whereas the other was expressed in cytoplasmic compartments. The authors suggested a complex mechanism of receptor translocation which might account for the modulation of cell proliferation (Postiglione et al, 2005).…”
Section: Discussionmentioning
confidence: 99%
“…Comparative analysis of the CD105 (endoglin) receptor expression of different human tumor cells indicated two protein pools, one of which accounted for receptor surface expression, whereas the other was expressed in cytoplasmic compartments. The authors suggested a complex mechanism of receptor translocation which might account for the modulation of cell proliferation (Postiglione et al, 2005).…”
Section: Discussionmentioning
confidence: 99%
“…29) In previous studies, normal human dermal fibroblasts (NHDF) and peripheral blood mononuclear cells (PBMC) have also been used as control normal cells to clarify tumor selectivity. [30][31][32] We also examined chalcone-induced cytotoxicity using NHDF cells, but all of the chalcones (1-8) showed cytotoxic effects against NHDF, as well as neuroblastoma cells, by MTT assay (data not shown). From these results, it seems difficult to explain the tumor selectivity solely by comparing a few types of normal cells in vitro.…”
Section: Discussionmentioning
confidence: 99%
“…Cell type-specific expression has further been observed in macrophages (5), T-cells (6), bone marrow cells (7), stromal cells (8), vascular smooth muscle cells (9), and different types of cancer cells (10). Endoglin is classified as a transforming growth factor-␤ (TGF-␤) 5 type III receptor that needs the TGF-␤ type II receptor (T␤RII) to bind to TGF-␤1 and TGF-␤3 (11), in contrast to betaglycan, the second TGF-␤ type III receptor (12).…”
mentioning
confidence: 97%