Premium
CTNNBIP1 downregulation is associated with tumor grade and viral infections in gastric adenocarcinoma
Author(s) -
KosariMonfared Mohadeseh,
Nikbakhsh Novin,
Fattahi Sadegh,
Ghadami Elham,
Ranaei Mohammad,
Taheri Hassan,
AmjadiMoheb Fatemeh,
Godazandeh Gholam A.,
Shafaei Shahryar,
PilehchianLangroudi Maryam,
Samadani Ali Akbar,
AkhavanNiaki Haleh
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27106
Subject(s) - biology , oncogene , cancer , carcinogenesis , helicobacter pylori , methylation , epigenetics , downregulation and upregulation , cancer research , dna methylation , adenocarcinoma , wnt signaling pathway , viral oncogene , tumor suppressor gene , immunology , gene expression , gene , genetics , cell cycle
Gastric cancer is a life‐threatening disease; resulting from interaction among genetic, epigenetic, and environmental factors. Aberrant dysregulation and methylation changes in Wnt/β‐catenin signaling downstream elements are a prevalent phenomenon encountered in gastric tumorigenesis. Also, viral infections play a role in gastric cancer development. CTNNBIP1 (β‐catenin interacting protein 1) gene is an antagonist of Wnt signaling which binds to the β‐catenin molecules. The CTNNBIP1 function as tumor suppressor gene or oncogene in different types of cancer is controversial. Moreover, its function and regulatory mechanisms in gastric cancer progression is unknown. In the present study, we examined CTNNBIP1 gene expression, the methylation status of the regulatory region of the gene, and their association with Epstein–Barr virus (EBV), and cytomegalovirus (CMV) and Helicobacter pylori infections in human gastric adenocarcinoma tissues in comparison with their adjacent nontumoral tissues. Our data revealed a significant downregulation of CTNNBIP1 in gastric tumors. Female patients showed lower level of CTNNBIP1 than males ( p < 0.05). Also, decreased expression of CTNNBIP1 was markedly associated with well‐differentiated tumor grades ( p < 0.05). No methylation change was observed between tumoral and nontumoral tissues. Additionally, CTNNBIP1 down regulation was significantly associated with CMV infection ( p < 0.05). In the absence of EBV infection, lower expression of CTNNBIP1 was observed. There was no association between H. pylori infection and CTNNBIP1 expression. Our findings revealed the tumor suppressor role for CTNNBIP1 in gastric adenocarcinoma. Interestingly, EBV and CMV infections modulate CTNNBIP1 expression.