choriocarcinoma/phosphatase

We compared microRNA profiles between choriocarcinoma and non-cancerous trophoblasts, and revealed that miR-199b was underexpressed in choriocarcinoma. By computational prediction and microarray studies, SET (protein phosphatase 2A inhibitor) was shown to be one of the target genes regulated by

The expression of human placental-type alkaline phosphatase (ALPase) in the placenta and in three choriocarcinoma cell lines was examined by translation in vitro and RNA blot analysis using a cDNA for placental ALPase. Placental RNA directed the synthesis of two polypeptides that could be

The coincident expression of two structurally distinct isoenzymes of human alkaline phosphatase was demonstrated in two independently derived gestational choriocarcinoma cell lines. These proteins were shown to have enzymatic, antigenic, and physical-chemical properties resembling those of

Treatment of the BeWo line of choriocarcinoma cells with methotrexate in doses that inhibit DNA synthesis causes a tenfold increase in synthesis of human chorionic gonadotropin and a threefold increase in activity of placental alkaline phosphatase. No concomitant increase in lactic dehydrogenase

A gastric choriocarcinoma cell line synthesizing human chorionic gonadotropin (HCG) was established in 1971 by Oboshi et al. and was found to possess human placental alkaline phosphatase. The present paper also deals with the relationship between the cell growth and HCG secretion and with cellular

Alkaline phosphatase (ALP) in human choriocarcinoma cells (malignant trophoblasts) was characterized by its greater sensitivity to EDTA and L-leucine inhibition as compared with the placental isozyme. In addition, both the fully processed and the nonglycosylated forms of choriocarcinoma ALP migrated

The alkaline phosphatase (AP) synthesized by human tumor cells closely resembles human placental AP (PLAP). Little is known about the molecular events that lead to the expression of a placenta-like AP in tumor cells. The complementary DNA encoding the AP expressed by a choriocarcinoma cell line,

Methotrexate (MTX) was covalently bound to rabbit antibodies (IgG) against hCG and placental alkaline phosphatase (PLALP) by two different methods. By carbodiimide method, 16.9 mols of MTX could be coupled to one mol of IgG, but the antibody activity was completely lost. Whereas, 2.6-3.4 mols of MTX

Alkaline phosphatase is induced in human choriocarcinoma cells by short-chain fatty acids, especially sodium butyrate. This fatty acid increases the phosphatase activity immediately and in a nearly linear fashion. Only phosphatase with an alkaline pH optimum is induced. Both the induced alkaline

Placental alkaline phosphatase (PLAP)-specific monoclonal antibody (MAb) 11-D-10, which did not react with other isoenzymes of alkaline phosphatase (AP), was raised by a hybridoma technique. MAb 11-D-10 was radiolabeled and administered to athymic mice bearing human choriocarcinoma containing PLAP.

Growth of choriocarcinoma cells in the presence of 5-bromo-2'-deoxyuridine (BrdUrd) results in a 30- to 40-fold increase in alkaline phosphatase activity. The effects of BrdUrd is specific for phosphatase with an alkaline pH optimum. The induction by BrdUrd is probably not due to the production of

The alkaline phosphatase activity expressed by JAR choriocarcinoma cells was compared to the placental isoenzyme of human alkaline phosphatase by several criteria. JAR cell alkaline phosphatase was similar to the placental isoenzyme with respect to heat and urea stability and sensitivity to most

BeWo choriocarcinoma cells synthesize two alkaline phosphatase isoenzymes: germ-cell alkaline phosphatase and tissue-unspecific alkaline phosphatase. We have made use of the differential heat-stabilities of these two isoenzymes to study the induction of germ-cell alkaline phosphatase by sodium

Expression of the germ cell alkaline phosphatase is a highly regulated process tied to malignant transformation of the human placenta. Human choriocarcinoma cells (malignant trophoblasts) express primarily the germ cell alkaline phosphatase gene and only low or nondetectable levels of the placental

Trophoblast cells (TBCs) form the blastocyst-derived component of the placenta and play essential roles in fetal maintenance. The proinflammatory cytokine IFN-gamma plays a central role in activating cellular immunity, controlling cell proliferation, and inducing apoptosis. IFN-gamma is secreted by