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. 2007 May-Jun;27(3B):1493-502.

Butyrate inhibits oral cancer cell proliferation and regulates expression of secretory phospholipase A2-X and COX-2

Yukako Miki  1 , Shotaro Mukae, Makoto Murakami, Yukio Ishikawa, Toshiharu Ishii, Hidero Ohki, Mitsuhiko Matsumoto, Kazuo Komiyama
Affiliations
  • PMID: 17595767
Free article

Butyrate inhibits oral cancer cell proliferation and regulates expression of secretory phospholipase A2-X and COX-2

Yukako Miki et al. Anticancer Res. 2007 May-Jun.
Free article

Abstract

Although surgical resection is the first choice for oral cancer, the development of new anti-cancer drugs is of great interest. The effect of the histone deacetylation inhibitor, sodium butyrate (NaBu) on oral cancer cell (OCC) HSC-3 and HSC-4 proliferation in vitro was investigated. The synthesis of rate-limiting enzymes such as sPLA2 (-IIA, -V, -X) and COX-2 was examined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot, as well as PGE2 by ELISA. NaBu acted in a concentration-dependent manner. Over 3 mM, it inhibited OCC proliferation, due to increased p21 expression and cell cycle arrest in the G2/M-phase. At low concentration (< or = 1 mM), NaBu showed no effects or enhanced cell proliferation. NaBu also regulated COX-2 and sPLA2-X expression, and augmented PGE2 synthesis in OCC. These results indicate that NaBu is a novel candidate agent for the treatment of oral cancer. The treatment efficacy must be investigated in additional experiments considering NaBu concentration and tumor cell heterogeneity.

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