A Histone Deacetylase Inhibitor, Trichostatin A, Enhances adiosensitivity by Abrogating G2/M Arrest in Human Carcinoma Cells
- Authors
- In Ah Kim; 김진호; Jin Hee Shin; Il Han Kim; 김재성; Hong-Gyun Wu; Eui Kyu Chie; Yong Ho Kim; Bo-Kyung Kim; Semie Hong; Seok Won Park; Sung Whan Ha; Charn Il Park
- Issue Date
- 2005
- Publisher
- 대한암학회
- Keywords
- Trichostatin A; Histone deacetylase inhibitor; Radiosensitization; G2/M arrest
- Citation
- Cancer Research and Treatment, v.37, no.2, pp 122 - 128
- Pages
- 7
- Journal Title
- Cancer Research and Treatment
- Volume
- 37
- Number
- 2
- Start Page
- 122
- End Page
- 128
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/47084
- ISSN
- 1598-2998
2005-9256
- Abstract
- Purpose: Histone deacetylase inhibitors (HDIs) are emerging as potentially useful components in anticancer therapy. In this study, we tried to confirm the radiosensitizing effect of richostatin A (TSA) on a panel of uman carcinoma cell lines and elucidate its mechanism of interaction.
Materials and Methods: A549, HeLa and Caski cells were exposed to TSA for 18 hr prior to irradiation, and the cell survival then measured using a clonogenic assay. Western blot and flow cytometric analyses, for histone acetylation, and cell cycle and apoptosis, respectively,were also performed.
Results: TSA increased the acetylation of histone H3. The pretreatment of TSA consistently radiosensitized all three cell lines. The SF2 (surviving fraction at 2 Gy) of TSA-treated cells was significantly lower than that of mock treated cells. The SER (sensitizer enhancement ratio) increased in all 3 cell lines, in concentration dependent manners. The TSA treated cells showed abrogation of radiation-induced G2/M arrest, in a concentration dependent manner.
Conclusion: The pretreatment of TSA enhanced the radiosensitivity of a panel of human carcinoma cells, which was attributed, in part, to the abrogation of radiationinduced G2/M arrest.
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