Effect of dietary apigenin on colonic ornithine decarboxylase activity, aberrant crypt foci formation, and tumorigenesis in different experimental models.

2.50
Hdl Handle:
http://hdl.handle.net/10146/53513
Title:
Effect of dietary apigenin on colonic ornithine decarboxylase activity, aberrant crypt foci formation, and tumorigenesis in different experimental models.
Authors:
Au, Angela; Li, Boyong; Wang, Weiqun; Roy, Hemant; Koehler, Ken; Birt, Diane
Abstract:
The efficacy of dietary apigenin, a dietary flavonoid, in colon cancer prevention was investigated by evaluating the inhibition of the ornithine decarboxylase (ODC) activity and the formation of aberrant crypt foci (ACF) and by studying the ability of apigenin to block colon carcinogenesis in two mouse models. First, the activity of ODC was measured in colon cancer cells (Caco-2) and in the colon epithelium of CF-1 mice. Apigenin at 10 and 30 muM significantly inhibited the ODC activity of Caco-2 cells by 26% and 57%, respectively. Colonic ODC activity in CF-1 mice was reduced with 0.1% dietary apigenin by 42% compared with the control, but this difference was not statistically significant. Second, ACF formation was evaluated in azoxymethane (AOM)-induced CF-1 mice. Female CF-1 mice at 6 wk of age were i.p. injected with 5 mg/kg body weight (BW) AOM once to induce ACF. ACF formation in CF-1 mice was reduced by 50% (P < 0.05) with 0.1% dietary apigenin fed for 6 wk when compared with the control. Dietary apigenin inhibited ACF only in the distal region of the CF-1 mouse colon. Finally, tumorigenesis studies were conducted using two different mouse models: AOM-induced CF-1 mice and Min mice with mutant adenomatous polyposis coli (APC) gene. Female CF-1 mice at 6 wk of age were i.p. injected with 10 mg/kg BW AOM weekly for 6 (AOM Study I) or 4 (AOM Study II) wk to induce tumors. CF-1 mice were fed diets containing 0.025% or 0.1% apigenin for 23-25 wk. Female Min mice were fed diets for 10 wk beginning at 5 wk of age. In two AOM-treated mouse colon tumor studies 0.025% and 0.1% dietary apigenin modestly reduced tumors in the group fed 0.025% apigenin (25% incidence in comparison with 65% in the controls) in a non-dose response manner. Apigenin failed to inhibit adenoma formation in the Min mouse study. These results suggest that dietary apigenin showed promise in cancer prevention by reducing the ODC activity and ACF formation, however, clear evidence of cancer prevention was not obtained in mouse tumor studies. Further investigation of the potential chemopreventive effect of apigenin in carcinogenesis is warranted.
Citation:
Nutr. Cancer 2006, 54 (2):243-251
Journal:
Nutrition and Cancer
Issue Date:
2006
URI:
http://hdl.handle.net/10146/53513
DOI:
10.1207/s15327914nc5402_11
PubMed ID:
16898869
Additional Links:
http://www.informaworld.com/smpp/content~content=a785829700~db=all~order=page
Type:
Article
Language:
en
Description:
Dietary modulation of cancer & cancer biomarkers; Dietary modulation of carcinogenesis-related pathways. Dietary item or component studied: apigenin Outcome studied: colon carcer risk; ornithine decarboxylase (ODC) activity; formation of aberrant crypt foci (ACF)Study type: colon cancer cells (Caco-2); CF-1 mice; Min mice Tissue/biological material/sample size: colon. Mode of exposure: dietary. Impact on outcome (including dose-response): Apigenin at 10 and 30 muM significantly inhibited the ODC activity of Caco-2 cells by 26% and 57%, respectively. Colonic ODC activity in CF-1 mice was reduced with 0.1% dietary apigenin by 42% compared with the control, but this difference was not statistically significant. ACF formation in CF-1 mice was reduced by 50% (P < 0.05) with 0.1% dietary apigenin fed for 6 wk when compared with the control. Dietary apigenin inhibited ACF only in the distal region of the CF-1 mouse colon. Female CF-1 mice at 6 wk of age were i.p. injected with 10 mg/kg BW AOM weekly for 6 (AOM Study I) or 4 (AOM Study II) wk to induce tumors. CF-1 mice were fed diets containing 0.025% or 0.1% apigenin for 23-25 wk. Female Min mice were fed diets for 10 wk beginning at 5 wk of age. In two AOM-treated mouse colon tumor studies 0.025% and 0.1% dietary apigenin modestly reduced tumors in the group fed 0.025% apigenin (25% incidence in comparison with 65% in the controls) in a non-dose response manner. Apigenin failed to inhibit adenoma formation in the Min mouse study.Keywords - classifictaion: administration & dosage;Animals;Apigenin;Azoxymethane;Caco-2 Cells;Carcinogens;chemically induced;Colon;Colonic Neoplasms;Diet;dietary modulation of cancer & cancer biomarkers;dietary modulation of carcinogenesis-related pathways;Disease Models,Animal;Dose-Response Relationship,Drug;drug effects;enzymology;Female;Food;Human;Humans;Iowa;metabolism;Mice;Mice,Inbred Strains;Ornithine Decarboxylase;pathology;pharmacology;Precancerous Conditions;prevention & control;Random Allocation;Research;toxicity;
ISSN:
0163-5581
Appears in Collections:
Articles with annotation

Full metadata record

DC FieldValue Language
dc.contributor.authorAu, Angela-
dc.contributor.authorLi, Boyong-
dc.contributor.authorWang, Weiqun-
dc.contributor.authorRoy, Hemant-
dc.contributor.authorKoehler, Ken-
dc.contributor.authorBirt, Diane-
dc.date.accessioned2009-03-10T08:45:05Z-
dc.date.available2009-03-10T08:45:05Z-
dc.date.issued2006-
dc.identifier.citationNutr. Cancer 2006, 54 (2):243-251en
dc.identifier.issn0163-5581-
dc.identifier.pmid16898869-
dc.identifier.doi10.1207/s15327914nc5402_11-
dc.identifier.urihttp://hdl.handle.net/10146/53513-
dc.descriptionDietary modulation of cancer & cancer biomarkers; Dietary modulation of carcinogenesis-related pathways. Dietary item or component studied: apigenin Outcome studied: colon carcer risk; ornithine decarboxylase (ODC) activity; formation of aberrant crypt foci (ACF)Study type: colon cancer cells (Caco-2); CF-1 mice; Min mice Tissue/biological material/sample size: colon. Mode of exposure: dietary. Impact on outcome (including dose-response): Apigenin at 10 and 30 muM significantly inhibited the ODC activity of Caco-2 cells by 26% and 57%, respectively. Colonic ODC activity in CF-1 mice was reduced with 0.1% dietary apigenin by 42% compared with the control, but this difference was not statistically significant. ACF formation in CF-1 mice was reduced by 50% (P < 0.05) with 0.1% dietary apigenin fed for 6 wk when compared with the control. Dietary apigenin inhibited ACF only in the distal region of the CF-1 mouse colon. Female CF-1 mice at 6 wk of age were i.p. injected with 10 mg/kg BW AOM weekly for 6 (AOM Study I) or 4 (AOM Study II) wk to induce tumors. CF-1 mice were fed diets containing 0.025% or 0.1% apigenin for 23-25 wk. Female Min mice were fed diets for 10 wk beginning at 5 wk of age. In two AOM-treated mouse colon tumor studies 0.025% and 0.1% dietary apigenin modestly reduced tumors in the group fed 0.025% apigenin (25% incidence in comparison with 65% in the controls) in a non-dose response manner. Apigenin failed to inhibit adenoma formation in the Min mouse study.Keywords - classifictaion: administration & dosage;Animals;Apigenin;Azoxymethane;Caco-2 Cells;Carcinogens;chemically induced;Colon;Colonic Neoplasms;Diet;dietary modulation of cancer & cancer biomarkers;dietary modulation of carcinogenesis-related pathways;Disease Models,Animal;Dose-Response Relationship,Drug;drug effects;enzymology;Female;Food;Human;Humans;Iowa;metabolism;Mice;Mice,Inbred Strains;Ornithine Decarboxylase;pathology;pharmacology;Precancerous Conditions;prevention & control;Random Allocation;Research;toxicity;en
dc.description.abstractThe efficacy of dietary apigenin, a dietary flavonoid, in colon cancer prevention was investigated by evaluating the inhibition of the ornithine decarboxylase (ODC) activity and the formation of aberrant crypt foci (ACF) and by studying the ability of apigenin to block colon carcinogenesis in two mouse models. First, the activity of ODC was measured in colon cancer cells (Caco-2) and in the colon epithelium of CF-1 mice. Apigenin at 10 and 30 muM significantly inhibited the ODC activity of Caco-2 cells by 26% and 57%, respectively. Colonic ODC activity in CF-1 mice was reduced with 0.1% dietary apigenin by 42% compared with the control, but this difference was not statistically significant. Second, ACF formation was evaluated in azoxymethane (AOM)-induced CF-1 mice. Female CF-1 mice at 6 wk of age were i.p. injected with 5 mg/kg body weight (BW) AOM once to induce ACF. ACF formation in CF-1 mice was reduced by 50% (P < 0.05) with 0.1% dietary apigenin fed for 6 wk when compared with the control. Dietary apigenin inhibited ACF only in the distal region of the CF-1 mouse colon. Finally, tumorigenesis studies were conducted using two different mouse models: AOM-induced CF-1 mice and Min mice with mutant adenomatous polyposis coli (APC) gene. Female CF-1 mice at 6 wk of age were i.p. injected with 10 mg/kg BW AOM weekly for 6 (AOM Study I) or 4 (AOM Study II) wk to induce tumors. CF-1 mice were fed diets containing 0.025% or 0.1% apigenin for 23-25 wk. Female Min mice were fed diets for 10 wk beginning at 5 wk of age. In two AOM-treated mouse colon tumor studies 0.025% and 0.1% dietary apigenin modestly reduced tumors in the group fed 0.025% apigenin (25% incidence in comparison with 65% in the controls) in a non-dose response manner. Apigenin failed to inhibit adenoma formation in the Min mouse study. These results suggest that dietary apigenin showed promise in cancer prevention by reducing the ODC activity and ACF formation, however, clear evidence of cancer prevention was not obtained in mouse tumor studies. Further investigation of the potential chemopreventive effect of apigenin in carcinogenesis is warranted.en
dc.language.isoenen
dc.relation.urlhttp://www.informaworld.com/smpp/content~content=a785829700~db=all~order=pageen
dc.subject.meshAnimals-
dc.subject.meshApigenin-
dc.subject.meshAzoxymethane-
dc.subject.meshCaco-2 Cells-
dc.subject.meshCarcinogens-
dc.subject.meshColon-
dc.subject.meshColonic Neoplasms-
dc.subject.meshDiet-
dc.subject.meshDisease Models, Animal-
dc.subject.meshDose-Response Relationship, Drug-
dc.subject.meshFemale-
dc.subject.meshHumans-
dc.subject.meshMice-
dc.subject.meshMice, Inbred Strains-
dc.subject.meshOrnithine Decarboxylase-
dc.subject.meshPrecancerous Conditions-
dc.subject.meshRandom Allocation-
dc.titleEffect of dietary apigenin on colonic ornithine decarboxylase activity, aberrant crypt foci formation, and tumorigenesis in different experimental models.en
dc.typeArticleen
dc.identifier.journalNutrition and Canceren
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