SUBCELLULAR LOCALIZATION OF BETA CATENIN IN COLORECTAL NON NEOPLASTIC AND NEOPLASTIC LESIONS
Abstract: Loss of adenomatous
polyposis coli (APC) function is typically an early event in sporadic colorectal cancer (CRC) pathogenesis.
The key tumor suppressor function of the APC
protein lies in its ability to destabilize free cytoplasmic beta
catenin. This lead to the accumulation of nuclear beta catenin, and together
with the DNA binding protein Tcf-4, function as a transcriptional activator.
Accumulation of stabilized free
β-catenin is considered as an early event and perhaps initiating the
process in intestinal tumorigenesis. Neoplastic transformation in the CRC
associated chronic colitis is considered similar to the adenoma-carcinoma
sequence in sporadic CRC. The distinguish feature from the CRC-related colitis
is the difference in time and frequency changes. Loss of APC function, regarded
as the beginning of a very common event in sporadic CRC, but the CRC associated
chronic colitis generally occurs at the end of the dysplasia-carcinoma
sequence. This research was conducted to determine the subcellular location of
beta catenin expression in chronic colitis, colorectal adenomas and carcinomas
that were evaluated by immunohistochemical staining. It can be concluded that
beta-catenin is a component that plays a role in the development of the CRC and
the subcellular location of beta-catenin can describe its oncogenic activity.
Author: Diah Rini Handjari,
Pamela Abineno, Budiningsih Siregar
Journal Code: jpkedokterangg110221
