Apigenin induced apoptosis through p53-dependent pathway in human cervical carcinoma cells.

Abstract

Apigenin is a widely distributed plant flavonoid and was proposed as an antitumor agent. In this study, we reported for the first time that apigenin inhibited the growth of human cervical carcinoma cells (HeLa) and through apoptotic pathway. The results showed that apigenin significantly decreased the viability of HeLa cells at 37-74 microM and the IC50 value was 35.89 microM. Apigenin-induced apoptosis in HeLa cells was confirmed by DNA fragmentation assay and induction of sub-G1 phase by flow cytometry. Apigenin-treated HeLa cells were arrested at G1 phase, which was associated with a marked increment of the expression of p21/WAF1 protein. The induction of p21/WAF1 appeared to be transcriptionally upregulated and was p53-dependent. In addition, apigenin induced Fas/APO-1 and caspase-3 expression which were also correlated with apoptosis. Apigenin decreased in the protein expression of Bcl-2 protein, which is an anti-apoptotic factor. The conclusion of this study is the apigenin induced p53 expression which caused cell cycle arrest and apoptosis. These findings suggest that apigenin has strong potential for development as an agent for preventing cervical cancer.

• Authors: Pei-Wen Zheng, Lien-Chai Chiang, Chun-Ching Lin
• Journal: Life sciences (Life Sci) Vol. 76 Issue 12 Pg. 1367-79 (Feb 04 2005) ISSN: 0024-3205 [Print] Netherlands
• PMID: 15670616 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• DNA-Binding Proteins
• Proto-Oncogene Proteins c-bcl-2
• TCEAL1 protein, human
• Transcription Factors
• Tumor Suppressor Protein p53
• fas Receptor
• Apigenin
• CASP3 protein, human
• Caspase 3
• Caspases

Topics

• Antineoplastic Agents (pharmacology)
• Apigenin (pharmacology)
• Apoptosis (drug effects)
• Caspase 3
• Caspases (biosynthesis)
• Cell Cycle (drug effects)
• Cell Survival (drug effects)
• DNA Fragmentation
• DNA-Binding Proteins (biosynthesis, genetics)
• Dose-Response Relationship, Drug
• Female
• HeLa Cells (drug effects, metabolism, pathology)
• Humans
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• Transcription Factors (biosynthesis, genetics)
• Tumor Suppressor Protein p53 (metabolism)
• fas Receptor (biosynthesis)