Document Type

Article

Publication Date

7-30-2008

Abstract

Hyperglycosylated human chorionic gonadotropin (hCG-H), a variant of hCG, has been shown to promote the growth and invasion of trophoblast cells in early pregnancy placental implantation, choriocarcinoma and testicular germ cell malignancies. In a previous study (15), hCG-H was found to have a significant effect on the growth of a choriocarcinoma cell line, JEG-3, and a testicular embroyonal carcinoma cell line, NTERA. It was also shown that, B152, an anti-hCG-H specific monoclonal antibody, significantly inhibited the growth of these cells in vitro and in vivo murine models. In this study, we quantified the amount of hCG-H produced by two embryonal carcinoma cell lines, n2102Ep and NTERA 2.clone D1 (NT2/D1). We then investigated the impact of B-152 on the proliferation of each cell line as well as JEG-3. Over a 72 hour period, n2102Ep was found to produce 0.04 mIU of hCG per 10,000 cells and 0.004 of hCG-H per 10,000 cells. The proportion of hCG-H produced by n2102Ep was 10.0%. NT2/D1 produced 0.02 mIU of hCG per 10,000 cells and 0.002 mIU of hCG-H per 10,000 cells. The proportion of hCG-H produced by NT2/D1 was 11.5%. We then cultured these cell lines and JEG-3 in seven different concentrations of B152 ranging from 0.0 μg/mL to 40 μg/mL for 72 hours. Cell proliferation was determined by measuring the absorbance of each cell line and determining a percentage of proliferation relative to a control without additional B152. Cell proliferation decreased with increasing concentrations of B152 for all three cell lines with significance determined by Bartholomews Test of increasing means: n2102Ep (P value <0.001), NT2/D1 (P value 0.005), and JEG-3 (P value 0.001). Results suggest that B152 had a negative effect on the cell proliferation of n2102Ep, NT2/D1, and JEG-3. We conclude that hyperglycosylated hCG appears to inhibit the growth of two embryonal carcinoma cell lines, n2102Ep and NT2/D1, and confirm earlier studies in which B-152 inhibited JEG-3 growth.'

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