Enzymatic activity of DNMT increased up to 220% in CTPE cells compared with control cells.
To study the mechanism of cadmiuminduced RASSF1A and p16 quiescence in CTPE cells, we assessed promoter region methylation.
Effect of procainamide on global DNA methylation and RASSF1A and p16 expression in control and CTPE cells.
DNMT1 inhibition only modestly increased both RASSF1A (23%) (Figure 6B) and p16 (28%) (Figure 6C) expression at the protein level in CTPE cells.
Increased expression of DNMT3b in CTPE cells occurred as an early event in response to chronic cadmium exposure, and, importantly, in advance of malignant transformation.
2006), but it is clearly required to maintain the aberrant DNA methylation in CTPE cells.
The CTPE cell line was developed by chronic cadmium exposure of the RWPE-1 cell line as previously described, and CTPE cells form aggressive, prostate carcinoma-like tumors upon inoculation into nude mice (Achanzar et al.
Continuous cadmium exposure for 8 or more weeks induces malignant transformation in RWPE-1 cells, producing the tumor-forming CTPE transformant (Achanzar et al.
CTPE cells acquire generalized resistance to chemically induced apoptosis.
All three MAPKs were phosphorylated in a cadmium concentration-dependent fashion both in control and CTPE cells.
Thus, studies were designed to determine if Ro318220 could bypass the blockage of JNK kinase activity in CTPE cells.
Thus, the transcriptional levels of Bcl-2 and Bax in CTPE and control were determined.