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...
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Published in | Journal of Medical Sciences Vol. 39; no. 2; pp. 61 - 66 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
台灣
國防醫學院
01.03.2019
Medknow Publications and Media Pvt. Ltd Wolters Kluwer Medknow Publications |
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Abstract | 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. |
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AbstractList | 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. 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. |
Audience | Academic |
Author | Ying-Chuan Chen Pei-Yao Liu |
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References | Lineberry (key-10.4103/1011-4564.242466-6) 2008 Lin (key-10.4103/1011-4564.242466-8) 2009 Lu (key-10.4103/1011-4564.242466-9) 2005 Petitjean (key-10.4103/1011-4564.242466-10) 2007 el-Deiry (key-10.4103/1011-4564.242466-12) 1993 Herbig (key-10.4103/1011-4564.242466-13) 2004 Su (key-10.4103/1011-4564.242466-7) 2006 Kriegel (key-10.4103/1011-4564.242466-2) 2009 Sperka (key-10.4103/1011-4564.242466-16) 2012 Muller (key-10.4103/1011-4564.242466-11) 2013 Abbas (key-10.4103/1011-4564.242466-15) 2009 Chen (key-10.4103/1011-4564.242466-17) 2013 Suh (key-10.4103/1011-4564.242466-18) 2011 Nurieva (key-10.4103/1011-4564.242466-3) 2010 Soares (key-10.4103/1011-4564.242466-4) 2004 Kumar (key-10.4103/1011-4564.242466-14) 2006 Anandasabapathy (key-10.4103/1011-4564.242466-1) 2003 Lineberry (key-10.4103/1011-4564.242466-5) 2008 |
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Snippet | 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:... 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... |
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SubjectTerms | Analysis Apoptosis Biochemistry Cancer Cancer cells Fluorescence Gene expression Genes Genetic aspects Grail MEDLINE Methylene blue Mouth cancer oral cancer cells p53 and p21 Polymerase chain reaction Scopus Tumor proteins Tumors |
Title | Grail Suppresses Stress‑induced Apoptosis and Colony Formation in Oral Cancer Cells |
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