ObjectiveTo understand the role of abnormal expression of P53 and P21 protein in oncogenesis and development of EBVaGCs and to analyze the relationship between EBV infection and P53 and P21 expression.
Results:P21 expression was not detected in normal cases and its positive rates were 60.00% , 10.00% , 40.00% , 15. 00% , 10.00% and 16.67% in cases of colorectal cancer, edge tissue of colorectal cancer, adenoma, phlogistic polipus, inflammatory ulcer and schistosmiasis respectively, a remarked difference was existed between cases of cancer and others( P < 0.05).
Synthesis of p53 and WAF1 (p21) proteins was studied in cells of patients with Nijmegen breakage syndrome (NBS) and of patients with ataxia telangiectasia (AT), as well as in normal cells with respect to their response to ionizing radiation (IR).
It may be concluded that sodium butyrate and trichostatin A could promote the proliferation/differentiation of the K562 cells, which might be contributed to the induced expression of cyclin D3 and p21 proteins.
Detection of ras oncogenes by analysis of p21 proteins in human tumor cell lines
The oncogenes code for the Ras p21 proteins, which localize in the internal part of the cell membrane and act as molecular switches to mediate downstream signaling from a variety of extracellular stimuli.
We have obtained evidence that oncogenic and activated normal ras-p21 proteins utilize overlapping but distinct signal transduction pathways.
It has been previously demonstrated that the virus did inhibit the growth of human hepatocarcinoma cell line PLC/PRF/5in vitro accompanied with the blockage of p21 expression.
The results showed that 17 cases were negative for p21 expression and 13 positive for p21.
Both sodium butyrate and trichostatin A could stimulate p21 expression of K562 cells at mRNA and protein levels.
The results showed that p21 expression, BrdU incorporation, and the mitotic index in uterine luminal epithelium increased 1 to 2 d after E2 stimulation and then declined to basal levels between d 3 and 6.
Furthermore, cotreatment with progesterone (P4) and E2 suppressed both p21 expression and the DNA synthesis stimulated by E2 alone in uterine epithelial cells.