Toxic and metabolic effect of sodium butyrate on SAS tongue cancer cells: role of cell cycle deregulation and redox changes.

5.00
Hdl Handle:
http://hdl.handle.net/10146/57573
Title:
Toxic and metabolic effect of sodium butyrate on SAS tongue cancer cells: role of cell cycle deregulation and redox changes.
Authors:
Jeng, Jiiang-Huei; Kuo, Mark Yen-Ping; Lee, Po-Hsuen; Wang, Ying-Jan; Lee, Mon-Ying; Lee, Jang-Jaer; Lin, Bor-Ru; Tai, Tseng-Fang; Chang, Mei-Chi
Abstract:
Butyrate is a metabolite produced by oral and colonic microorganism. Butyrate has been shown to reduce colon cancer, whereas its role in oral carcinogenesis is not clear. Butyrate concentration in dental plaque and saliva ranged from 0.2 to 16 mM. In this study, we found that sodium butyrate inhibited the growth of SAS tongue cancer cells by 32% and 53% at concentrations of 1 and 2mM, respectively. Low concentrations of sodium butyrate (1-8mM) induced G0/G1 cell cycle arrest of SAS cells, whereas concentrations of 4-16 mM elicited G2/M arrest and a slight increase in apoptotic cell populations. These events were concomitant with induction of intracellular reactive oxygen species (ROS) production. An elevation in p21 mRNA and protein level was noted in SAS cells by sodium butyrate. On the contrary, a decline of cyclin Bl, cdc2 and cdc25C mRNA and protein expression in SAS cells was found after exposure to sodium butyrate. In addition, no evident increase in cdc2 inhibitory phosphorylation was found in sodium butyrate-treated SAS cancer cells. Inclusion of N-acetyl-l-cysteine (NAC) (3mM), catalase (1000 U/ml) and dimethylthiourea (DMT, 5mM), and also SOD (500 U/ml) attenuated the sodium butyrate-induced ROS production in SAS cells. However, they were not able to prevent the cell cycle arrest, apoptosis and growth inhibition in SAS cells induced by 1, 2 and 16 mM of sodium butyrate. These results indicate that sodium butyrate is toxic and inhibits the tongue cancer cell growth via induction of cell cycle arrest and apoptosis. Sodium butyrate mediates these events by mechanisms additional to ROS production.
Citation:
Toxicology 2006, 223 (3):235-247
Journal:
Toxicology
Issue Date:
15-Jun-2006
URI:
http://hdl.handle.net/10146/57573
DOI:
10.1016/j.tox.2006.04.033
PubMed ID:
16737765
Additional Links:
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCN-4JTPM8R-B&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000055040&_version=1&_urlVersion=0&_userid=1843694&md5=c437c2f377737806f91bbf75cddf1089
Type:
Article
Language:
en
Description:
Lifestyle element evaluated: sodium butyrate. Outcome studied: toxic effect of sodium butyrate (cell cycle arrest, apoptosis and growth inhibition) in SAS tongue cancer cells; sodium butyrate-induced ROS production in SAS tongue cancer cells. Method of biomarker analysis: toxic effect of sodium butyrate on SAS cancer cells (growth of SAS cancer cells, cell cycle progression of SAS cancer cells); ROS production (Reactive oxygen species scavenging properties of sodium butyrate, effect of sodium butyrate on GSH and ROS levels in SAS cancer cells)Study type: Human tongue cancer cell line SAS Quality control: More than four separate experiments were performed for each test.Impact on outcome: Sodium butyrate inhibited the growth of SAS tongue cancer cells by 32% and 53% at concentrations of 1 and 2mM, respectively. Low concentrations of sodium butyrate (1-8mM) induced G0/G1 cell cycle arrest of SAS cells, whereas concentrations of 4-16 mM elicited G2/M arrest and a slight increase in apoptotic cell populations. These events were concomitant with induction of intracellular reactive oxygen species (ROS) production. An elevation in p21 mRNA and protein level was noted in SAS cells by sodium butyrate. On the contrary, a decline of cyclin Bl, cdc2 and cdc25C mRNA and protein expression in SAS cells was found after exposure to sodium butyrate. In addition, no evident increase in cdc2 inhibitory phosphorylation was found in sodium butyrate-treated SAS cancer cells. Inclusion of N-acetyl-l-cysteine (NAC) (3mM), catalase (1000 U/ml) and dimethylthiourea (DMT, 5mM), and also SOD (500 U/ml) attenuated the sodium butyrate-induced ROS production in SAS cells. However, they were not able to prevent the cell cycle arrest, apoptosis and growth inhibition in SAS cells induced by 1, 2 and 16 mM of sodium butyrate. KEYWORDS - CLASIFFICATION: analysis;Apoptosis;Butyrates;Cell Cycle;Cell Cycle Proteins;Cell Line,Tumor;drug effects;Free Radical Scavengers;Gene Expression;genetics;Human;Humans;lifestyle modulation of cancer & cancer biomarkers;mechanisms of carcinogenesis;metabolism;Oxidation-Reduction;pathology;pharmacology;Proteins;Reactive Oxygen Species;Research;Sodium;Taiwan;Tongue Neoplasms;Toxicology;
ISSN:
0300-483X
Appears in Collections:
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Full metadata record

DC FieldValue Language
dc.contributor.authorJeng, Jiiang-Huei-
dc.contributor.authorKuo, Mark Yen-Ping-
dc.contributor.authorLee, Po-Hsuen-
dc.contributor.authorWang, Ying-Jan-
dc.contributor.authorLee, Mon-Ying-
dc.contributor.authorLee, Jang-Jaer-
dc.contributor.authorLin, Bor-Ru-
dc.contributor.authorTai, Tseng-Fang-
dc.contributor.authorChang, Mei-Chi-
dc.date.accessioned2009-03-27T11:27:40Z-
dc.date.available2009-03-27T11:27:40Z-
dc.date.issued2006-06-15-
dc.identifier.citationToxicology 2006, 223 (3):235-247en
dc.identifier.issn0300-483X-
dc.identifier.pmid16737765-
dc.identifier.doi10.1016/j.tox.2006.04.033-
dc.identifier.urihttp://hdl.handle.net/10146/57573-
dc.descriptionLifestyle element evaluated: sodium butyrate. Outcome studied: toxic effect of sodium butyrate (cell cycle arrest, apoptosis and growth inhibition) in SAS tongue cancer cells; sodium butyrate-induced ROS production in SAS tongue cancer cells. Method of biomarker analysis: toxic effect of sodium butyrate on SAS cancer cells (growth of SAS cancer cells, cell cycle progression of SAS cancer cells); ROS production (Reactive oxygen species scavenging properties of sodium butyrate, effect of sodium butyrate on GSH and ROS levels in SAS cancer cells)Study type: Human tongue cancer cell line SAS Quality control: More than four separate experiments were performed for each test.Impact on outcome: Sodium butyrate inhibited the growth of SAS tongue cancer cells by 32% and 53% at concentrations of 1 and 2mM, respectively. Low concentrations of sodium butyrate (1-8mM) induced G0/G1 cell cycle arrest of SAS cells, whereas concentrations of 4-16 mM elicited G2/M arrest and a slight increase in apoptotic cell populations. These events were concomitant with induction of intracellular reactive oxygen species (ROS) production. An elevation in p21 mRNA and protein level was noted in SAS cells by sodium butyrate. On the contrary, a decline of cyclin Bl, cdc2 and cdc25C mRNA and protein expression in SAS cells was found after exposure to sodium butyrate. In addition, no evident increase in cdc2 inhibitory phosphorylation was found in sodium butyrate-treated SAS cancer cells. Inclusion of N-acetyl-l-cysteine (NAC) (3mM), catalase (1000 U/ml) and dimethylthiourea (DMT, 5mM), and also SOD (500 U/ml) attenuated the sodium butyrate-induced ROS production in SAS cells. However, they were not able to prevent the cell cycle arrest, apoptosis and growth inhibition in SAS cells induced by 1, 2 and 16 mM of sodium butyrate. KEYWORDS - CLASIFFICATION: analysis;Apoptosis;Butyrates;Cell Cycle;Cell Cycle Proteins;Cell Line,Tumor;drug effects;Free Radical Scavengers;Gene Expression;genetics;Human;Humans;lifestyle modulation of cancer & cancer biomarkers;mechanisms of carcinogenesis;metabolism;Oxidation-Reduction;pathology;pharmacology;Proteins;Reactive Oxygen Species;Research;Sodium;Taiwan;Tongue Neoplasms;Toxicology;en
dc.description.abstractButyrate is a metabolite produced by oral and colonic microorganism. Butyrate has been shown to reduce colon cancer, whereas its role in oral carcinogenesis is not clear. Butyrate concentration in dental plaque and saliva ranged from 0.2 to 16 mM. In this study, we found that sodium butyrate inhibited the growth of SAS tongue cancer cells by 32% and 53% at concentrations of 1 and 2mM, respectively. Low concentrations of sodium butyrate (1-8mM) induced G0/G1 cell cycle arrest of SAS cells, whereas concentrations of 4-16 mM elicited G2/M arrest and a slight increase in apoptotic cell populations. These events were concomitant with induction of intracellular reactive oxygen species (ROS) production. An elevation in p21 mRNA and protein level was noted in SAS cells by sodium butyrate. On the contrary, a decline of cyclin Bl, cdc2 and cdc25C mRNA and protein expression in SAS cells was found after exposure to sodium butyrate. In addition, no evident increase in cdc2 inhibitory phosphorylation was found in sodium butyrate-treated SAS cancer cells. Inclusion of N-acetyl-l-cysteine (NAC) (3mM), catalase (1000 U/ml) and dimethylthiourea (DMT, 5mM), and also SOD (500 U/ml) attenuated the sodium butyrate-induced ROS production in SAS cells. However, they were not able to prevent the cell cycle arrest, apoptosis and growth inhibition in SAS cells induced by 1, 2 and 16 mM of sodium butyrate. These results indicate that sodium butyrate is toxic and inhibits the tongue cancer cell growth via induction of cell cycle arrest and apoptosis. Sodium butyrate mediates these events by mechanisms additional to ROS production.en
dc.language.isoenen
dc.relation.urlhttp://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCN-4JTPM8R-B&_user=1843694&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000055040&_version=1&_urlVersion=0&_userid=1843694&md5=c437c2f377737806f91bbf75cddf1089en
dc.subjectAntioxidantsen
dc.subjectApoptosisen
dc.subjectButyrateen
dc.subjectCell cycleen
dc.subjectCytotoxicityen
dc.subjectReactive oxygen speciesen
dc.subject.meshApoptosis-
dc.subject.meshButyrates-
dc.subject.meshCell Cycle-
dc.subject.meshCell Cycle Proteins-
dc.subject.meshCell Line, Tumor-
dc.subject.meshFree Radical Scavengers-
dc.subject.meshGene Expression-
dc.subject.meshHumans-
dc.subject.meshOxidation-Reduction-
dc.subject.meshReactive Oxygen Species-
dc.subject.meshTongue Neoplasms-
dc.titleToxic and metabolic effect of sodium butyrate on SAS tongue cancer cells: role of cell cycle deregulation and redox changes.en
dc.typeArticleen
dc.identifier.journalToxicologyen

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