Abstract
In many kinds of cancers, 14-3-3sigma, one of the cell cycle negative regulator, is inactivated by hypermethylation of the gene. In colorectal cancers, this study revealed that the hypermethylation of the 14-3-3sigma gene was an uncommon event and 14-3-3sigma expression was kept even in established colorectal cancer cell lines. Immunohistochemical study using surgical materials showed the expression of 14-3-3sigma was localized at the deep peripheral area of the tumor, so-called invasion front. According to the results of Ki-67 and cyclin B1 immunohistochemistry, 14-3-3sigma-positive cases maintained higher proliferative activity compared to 14-3-3sigma-negative cases at IF. However, a significant correlation between 14-3-3sigma expression and proliferative activity in CRC cells remains to be unsolved.
MeSH terms
-
14-3-3 Proteins
-
Biomarkers, Tumor / genetics*
-
Biomarkers, Tumor / metabolism
-
Cell Cycle*
-
Colorectal Neoplasms / genetics*
-
Colorectal Neoplasms / metabolism
-
Cyclin B / metabolism
-
Cyclin B1
-
DNA Methylation*
-
DNA, Neoplasm / metabolism
-
Exonucleases / genetics*
-
Exonucleases / metabolism
-
Exoribonucleases
-
Gene Expression Regulation, Neoplastic*
-
Humans
-
Immunoenzyme Techniques
-
In Situ Hybridization
-
Ki-67 Antigen / metabolism
-
Neoplasm Invasiveness
-
Neoplasm Proteins / genetics*
-
Neoplasm Proteins / metabolism
-
RNA Probes
-
Tumor Cells, Cultured
-
Tumor Suppressor Protein p53 / metabolism
Substances
-
14-3-3 Proteins
-
Biomarkers, Tumor
-
CCNB1 protein, human
-
Cyclin B
-
Cyclin B1
-
DNA, Neoplasm
-
Ki-67 Antigen
-
Neoplasm Proteins
-
RNA Probes
-
Tumor Suppressor Protein p53
-
Exonucleases
-
Exoribonucleases
-
SFN protein, human