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ID 113603
Title Alternative
ANTITUMOUR EFFECT OF VALPROIC ACID AGAINST SALIVARY GLAND CANCER
Author
Nagai, Hirokazu The University of Tokushima KAKEN Search Researchers
Ohe, Go The University of Tokushima KAKEN Search Researchers
Hara, Kanae The University of Tokushima
Uchida, Daisuke The University of Tokushima KAKEN Search Researchers
Tamatani, Tetsuya The University of Tokushima KAKEN Search Researchers
Fujisawa, Kenji The University of Tokushima KAKEN Search Researchers
Keywords
valproic acid
salivary gland cancer
antitumour activity
epigenetics
histone deacetylase inhibitor
Content Type
Journal Article
Description
Salivary gland cancer (SGC) has a comparatively poor prognosis and is prone to frequent recurrence and metastases. Therefore, the development of more effective chemotherapy against SGC is desirable. The aim of the present study was to investigate the antitumour effects of valproic acid (VPA) against SGC in vitro and in vivo. Two human SGC cell lines (HSY and HSG cells) were used in the present study. The effects of VPA on the proliferation of SGC cells in vitro were assessed by MTT assay. Cancer cells treated with VPA were subjected to cell cycle analysis by flow cytometry. In addition, the expression levels of p21 and p27 were examined by real-time RT-PCR to identify the mechanisms of the antitumour effect of VPA on SGC. The effects of VPA on cancer growth in vivo were evaluated in a xenograft model. VPA inhibited the proliferation of SGC cells in a dose-dependent manner in vitro. Degenerated cancer cells were observed at high concentrations of VPA. In the cell cycle analysis, VPA induced cell-growth inhibition and G1 arrest of cell cycle progression in both cancer cell lines in a time-and dose-dependent manner. VPA markedly upregulated the mRNA expression levels of both p21 and p27 in both SGC cell lines in a time-dependent manner. In the xenograft model experiment, VPA treatment markedly inhibited the growth of salivary gland tumours when compared with the growth of the untreated controls. VPA may be a valuable drug in the development of better therapeutic regimens for SGC.
Journal Title
Oncology Reports
ISSN
1021335X
17912431
NCID
AA11016405
Publisher
Spandidos Publications
Volume
31
Issue
3
Start Page
1453
End Page
1458
Published Date
2013-12-31
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Oral Sciences
University Hospital