- 著者
- Yui Fujiwara Takahisa Murofushi Ryosuke Koshi Yoshikazu Mikami Hiromasa Tsuda
- 出版者
- Nihon University School of Dentistry
- 雑誌
- Journal of Oral Science (ISSN:13434934)
- 巻号頁・発行日
- pp.20-0411, (Released:2020-12-30)
- 参考文献数
- 9
- 被引用文献数
- 4
Treating the gingival epithelial Ca9-22 cell with butyrate, a short-chain fatty acid (SCFA) produced by bacteria within mature dental plaque, induces necrotic cellular death. In this report, it was examined whether SCFA-mediated cellular death is accompanied by a release of damage-associated molecular patterns (DAMPs). In addition, the role of reactive oxygen species (ROS) in the release of DAMPs was evaluated. Human gingival epithelial Ca9-22 cells were treated with butyrate or propionate. The amounts of dead cells were then measured using SYTOX-green dye. Released DAMPs were detected by western blot. The role of ROS scavengers, ascorbic acid and N-acetylcysteine, on DAMP-release was evaluated. Dose and time-dependent induction of Ca9-22 cell death was observed during butyrate and propionate treatments. This was accompanied by the release of DAMPs. Ascorbic acid or N-acetylcysteine reduced cellular death and inhibited DAMP-release induced by exposure to butyrate or propionate. These data collectively suggest that SCFA-induced death of gingival epithelial Ca9-22 cells and accompanying release of DAMPs are dependent on ROS.
- 著者
- Takahisa Murofushi Hiromasa Tsuda Yoshikazu Mikami Yoko Yamaguchi Naoto Suzuki
- 出版者
- 日本大学歯学部
- 雑誌
- Journal of Oral Science (ISSN:13434934)
- 巻号頁・発行日
- vol.59, no.3, pp.415-423, 2017 (Released:2017-09-14)
- 参考文献数
- 57
- 被引用文献数
- 8
SIRT1 is a NAD-dependent histone deacetylase that is important in a wide variety of physiological and pathophysiological processes. Although many studies have examined the relationship between SIRT1 and cancer, the role of SIRT1 in tumor malignancy is controversial. Here, we examined the effects of the SIRT1 activator CAY10591 in gingival epithelial carcinoma Ca9-22 cells. CAY10591 treatment dose- and time-dependently increased SIRT1 level and activity. The treatment decreased cell growth and induced cell-cycle repressor p21 levels. In addition, dimethyl sulfoxide significantly reduced cellular invasion and migration, and CAY10591 enhanced this decrease. Quantitative PCR analysis showed that CAY10591 decreased expression of several invasion/migration promoter genes and induced repressor genes. Our findings suggest that CAY10591 suppresses cell growth and invasion/migration activity in gingival squamous cell carcinoma Ca9-22 cells.