Publication: Molecular targets of apigenin in colorectal cancer cells: Involvement of p21, NAG-1 and p53
1
0
Issued Date
2010
Resource Type
File Type
application/pdf
ISSN
9598049
Other identifier(s)
2-s2.0-78649635941
Rights Holder(s)
Scopus
Bibliographic Citation
European Journal of Cancer. Vol 46, No.18 (2010), p.3365-3374
Suggested Citation
Zhong Y., Krisanapun C., Lee S.-H., Nualsanit T., Sams C., Peungvicha P., Baek S.J. Molecular targets of apigenin in colorectal cancer cells: Involvement of p21, NAG-1 and p53. European Journal of Cancer. Vol 46, No.18 (2010), p.3365-3374. doi:10.1016/j.ejca.2010.07.007 Retrieved from: https://hdl.handle.net/20.500.14740/7498
Abstract
Persuasive epidemiological and experimental evidence suggests that dietary flavonoids have anti-cancer activity. Since conventional therapeutic and surgical approaches have not been able to fully control the incidence and outcome of most cancer types, including colorectal neoplasia, there is an urgent need to develop alternative approaches for the management of cancer. We sought to develop the best flavonoids for the inhibition of cell growth, and apigenin (flavone) proved to be the most promising compound in colorectal cancer cell growth arrest. Subsequently, we found that pro-apoptotic proteins (NAG-1 and p53) and cell cycle inhibitor (p21) were induced in the presence of apigenin, and kinase pathways, including PKCδ and ataxia telangiectasia mutated (ATM), play an important role in activating these proteins. The data generated by in vitro experiments were confirmed in an animal study using APC MIN+ mice. Apigenin is able to reduce polyp numbers, accompanied by increasing p53 activation through phosphorylation in animal models. Our data suggest apparent beneficial effects of apigenin on colon cancer. © 2010 Elsevier Ltd. All rights reserved.
Subject(s)
Antineoplastic agent
Apigenin
ATM protein
Protein
Protein kinase C gamma
Protein nag 1
Protein p21
Protein p53
Unclassified drug
Animal experiment
Animal model
Antineoplastic activity
Article
Cancer cell
Colorectal cancer
Controlled study
Enzyme activation
Human
Human cell
In vitro study
Liquid chromatography
Mouse
Nonhuman
Priority journal
Protein expression
Protein phosphorylation
Reverse transcription polymerase chain reaction
Signal transduction
Transient transfection
Western blotting
Animals
Antineoplastic Agents
Apigenin
Apoptosis
Cell Proliferation
Colorectal Neoplasms
Cyclin-Dependent Kinase Inhibitor p21
Enzyme Inhibitors
Growth Differentiation Factor 15
Humans
Mice
Phosphorylation
Phosphotransferases
Tumor Cells, Cultured
Tumor Suppressor Protein p53
Apigenin
ATM protein
Protein
Protein kinase C gamma
Protein nag 1
Protein p21
Protein p53
Unclassified drug
Animal experiment
Animal model
Antineoplastic activity
Article
Cancer cell
Colorectal cancer
Controlled study
Enzyme activation
Human
Human cell
In vitro study
Liquid chromatography
Mouse
Nonhuman
Priority journal
Protein expression
Protein phosphorylation
Reverse transcription polymerase chain reaction
Signal transduction
Transient transfection
Western blotting
Animals
Antineoplastic Agents
Apigenin
Apoptosis
Cell Proliferation
Colorectal Neoplasms
Cyclin-Dependent Kinase Inhibitor p21
Enzyme Inhibitors
Growth Differentiation Factor 15
Humans
Mice
Phosphorylation
Phosphotransferases
Tumor Cells, Cultured
Tumor Suppressor Protein p53
