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World J Gastroenterol. Aug 7, 2007; 13(29): 4015-4018
Published online Aug 7, 2007. doi: 10.3748/wjg.v13.i29.4015
Possible mechanism for the regulation of glucose on proliferation, inhibition and apoptosis of colon cancer cells induced by sodium butyrate
Lei He, Xi Li, He-Sheng Luo, Han Rong, Jia Cai
Lei He, He-Sheng Luo, Jia Cai, Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
Xi Li, Department of Gastroenterology, Peking University Shenzhen Hospital, Shenzhen 518036, Guangdong Province, China
Han Rong, Department of Psychiatry, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Supported by the Key Technologies R&D Program of Hubei Province, No. 2004AA304B08
Correspondence to: He-Sheng Luo, Department of Gastro-enterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China. heleiyoyo@hotmail.com
Telephone: +86-27-61054272
Received: March 12, 2007
Revised: March 18, 2007
Accepted: March 31, 2007
Published online: August 7, 2007
Abstract

AIM: To study the effect of glucose on sodium butyrate-induced proliferation inhibition and apoptosis in HT-29 cell line, and explored its possible mechanisms.

METHODS: HT-29 cells were grown in RPMI-1640 medium supplemented with 10% fetal calf serum, and were allowed to adhere for 24 h, and then replaced with experimental medium. Cell survival rates were detected by MTT assay. Apoptosis was detected by TUNEL assay. Glucose transport protein 1 (GLUT1) and monocarboxylate transporter 1 (MCT1) mRNA expression was detected by RT-PCR.

RESULTS: Low concentration of glucose induced apoptosis and regulated proliferation in HT-29 cell line, and glucose can obviously inhibit the effect of proliferation inhibition and apoptosis induced by sodium butyrate. Glucose also down-regulated the expression of MCT1mRNA (0.28 ± 0.07 vs 0.19 ± 0.10, P < 0.05), and decreased the expression of GLUT1mRNA slightly (0.18 ± 0.04 vs 0.13 ± 0.03, P < 0.05).

CONCLUSION: Glucose can regulate the effect of proliferation inhibition and apoptosis induced by sodium butyrate and this influence may be associated with the intracellular concentration of glucose and sodium butyrate.

Keywords: Sodium butyrate, Glucose, Glucose transporter 1, Monocarboxylate transporter 1