We also observed a significant increase in ERCC1 expression, and decrease in p53 and EGFR expression, in EC-9706 cells treated with SNX-2112 (P < 0.05), indicating the regulation of EC by SNX-2112.
Inactivated tumor suppressor genes, including p53, often are suggested by loss of heterozygosity (LOH) studies. p53 gene inactivation has been reported in esophageal cancers.
Zerumbone can inhibit the proliferation and induce apoptosis of esophageal cancer EC-109 cells, and its induction of apoptosis may be realized through upregulating the mRNA expression of P53 and downregulating the mRNA expression of Bcl-2, and upregulating the protein expression of P53 and downregulating the protein expression of Bcl-2.
The vast majority of esophageal cancers have inactivation of the p53 and p16 genes at an early stage followed by defects in genes such as APC, Rb and cyclin D1 at later stages of progression.
These results suggest that HPV-16 and -18 may play a role in the pathogenesis of esophageal SCC, particularly with regard to its striking geographical distribution; that esophageal cancers do occur in the absence of HPV infection when over-expression of p53 is present; and that the presence of HPV infection and over-expression of p53 may each be a factor indicating a relatively poor prognosis.
Increased DNA content and heteroploid rate, accumulation of p53 protein, and over-expression of p21, telomerase and cyclin D1 proteins were early molecular events during the development of esophageal cancer.
We searched PubMed, Ovid MEDLINE, Embase, and Current Contents Connect to identify studies published between January 1990 and February 2016 of esophageal cancer populations that measured p53 expression and/or mutation status and reported hazard ratios (HRs), or adequate data for estimation of HRs for survival for p53-defined subgroups.
To identify HPV infection and p53 overexpression in oesophageal cancer, we performed immunohistochemical analysis using CM-1 anti-p53 antibody and DNA in situ hybridization with biotinylated HPV DNA probes on paraffin-embedded sections in 36 patients with oesophageal squamous cell carcinomas derived from a high-incidence area in northern China.
The purpose of this study is to test whether inhibition of beta-catenin or overexpression of p53 can decrease survivin expression and render esophageal cancer cells more susceptible to apoptosis.