Rap1 reverses transcriptional repression of TGF-beta type II receptor by a mechanism involving AP-1 in the human pancreatic cancer cell line, UK Pan-1.

The TGF-beta signaling pathway has potent anti-mitogenic effects in epithelial cells and loss of negative growth regulation is often associated with increased tumorigenicity. The human pancreatic ductal adenocarcinoma cell line, UK Pan-1, which expresses DPC4, is not highly responsive to TGF-beta due to transcriptional repression of TGF-beta type II receptor (RII). Here, we show that UK Pan-1 cells transfected with a plasmid to overexpress rap1 protein (UK/rap1) causes an increase in RII transcription and restores sensitivity to TGF-beta growth inhibition.

Characterization of a newly established human pancreatic carcinoma cell line, UK Pan-1.

Background: A highly tumorigenic cell line designated as UK Pan-1 was established in a surgically removed human pancreatic adenocarcinoma and characterized as having many of the genotypic and phenotypic alterations commonly found in pancreatic tumors.

Methods: The cell line was characterized by its morphology, growth rate in monolayer culture and soft agar, tumorigenicity in nude mice, and chromosomal analysis. Furthermore, the status of p53, Ki-ras mutation and transforming growth factor (TGF)-/receptor expression were determined.

Change in morphology of corpora lutea, central luteal cavities and steroid secretion patterns of postpartum suckled beef cows after melengestrol acetate with or without prostaglandin F2alpha.

Change in morphology of the corpus luteum (CL) and patterns of progesterone and estradiol secretion after treatment with melengestrol acetate (MGA) were monitored in postpartum beef cows. Twenty Angus cows were randomly assigned to MGA or MGA + prostaglandin F(2alpha) (PGF) treatments. All cows were fed 0.