Grail suppresses stress-induced apoptosis and colony formation in oral cancer cells

Aims: The purpose of this study is to investigate the role of Grail in stress-induced apoptosis and tumorigenesis in oral cancer cells. Subjects and Methods: We analyzed gene expression of Grail in oral cancer cell lines (KB, SAS, SCC-4, and SCC-25) treated with 5-azadC or/and trichostatin A (TSA) b...

Full description

Bibliographic Details
Main Authors: Pei-Yao Liu, Ying-Chuan Chen
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2019-01-01
Series:Journal of Medical Sciences
Subjects:
Online Access:http://www.jmedscindmc.com/article.asp?issn=1011-4564;year=2019;volume=39;issue=2;spage=61;epage=66;aulast=Liu
Description
Summary:Aims: The purpose of this study is to investigate the role of Grail in stress-induced apoptosis and tumorigenesis in oral cancer cells. Subjects and Methods: We analyzed gene expression of Grail in oral cancer cell lines (KB, SAS, SCC-4, and SCC-25) treated with 5-azadC or/and trichostatin A (TSA) by RT-PCR. The effects of Grail on the expression of p53 and p21 were analyzed by real-time polymerase chain reaction and Western blot for KB cells (KB/vector, KB/Grail and KB/shGrail). The anti-apoptotic effects of Grail were determined by fluorescence-activated cell sorting in KB/vector and KB/Grail cells. The effects of Grail on tumorigenesis were through clonogenic analysis in KB cells (KB/vector, KB/Grail and KB/shGrail). Results: Treatment with 5-azadC or/and TSA-induced Grail mRNA expression in oral cancer cells. Grail overexpression reduced p53 and p21 expression. Conversely, p53 and p21 expressions were increased in KB/shGrail cells. Furthermore, Grail can inhibit resveratrol-or etoposide-induced apoptosis in KB cells. Finally, Grail can significantly suppress colony formation in KB cells. Conclusions: The expression of Grail is epigenetically regulated in oral cancer cells. Grail can reduce p53 and p21 expression and stress-induced cell death and suppress the colony formation in KB cells.
ISSN:1011-4564