Apigenin is a natural occurring, ubiquitous, low molecular weight, bioactive plant flavone. It belongs to the flavonoid subclass and has antioxidant, anticancer, and anti-inflammatory properties. Apigenin affects several critical pathways and/or targets which are associated with several health disorders including cancer.
| Mechanism of Action | Apigenin exerts a broad range of molecular signaling effects. Apigenin is an ornithine decarboxylase inhibitor, which is involved in tumor growth and production. Polyphenols may affect the molecular events involved in initiation, promotion, and progression stages of carcinogenesis. Apigenin also has been shown to inhibit nitric oxide synthase-2 and cyclooxygenase-2 activity in mouse macrophages. Apigenin has been shown to increase the intracellular concentration of glutathione, enhancing the endogenous defense against oxidative stress. |
| Eukaryotic Cell Culture Applications | A number of the biological effects of Apigenin in numerous in vitro and in vivo mammalian systems are related to its antioxidant effects and its role in scavenging free radicals. It exhibits anti-mutagenic, anti-inflammatory, and antiviral effects (Yang et al, 2001).
Apigenin has been shown to possess anti-mutagenic properties in a setting of nitropyrene-induced genotoxicity in CHO cells. (Kuo et al, 1992). Apigenin exerts its effects on the cell cycle. Exposure of a wide array of malignant cells, including epidermal cells and fibroblasts to apigenin induced a reversible G2/M and G0/G1 arrest by inhibiting p34 (cdc2) kinase activity, accompanied by increased p53 protein stability (Plaumann et al, 1996). Apigenin has been reported to inhibit protein kinase C activity, mitogen activated protein kinase (MAPK), transformation of C3HI mouse embryonic fibroblasts and the downstream oncogenes in v-Ha-ras-transformed NIH3T3 cells (Lee et al, X) Apigenin promotes chelation of metals, and scavenges free radicals in both in vitro and in vivo tumor models (Middleton et al, 2000). |
| Cancer Applications | There is considerable potential for Apigenin to be developed as a cancer chemopreventive agent.
Apigenin has shown promise in inhibiting tumor cell invasion and metastases by regulating protease production (Lindenmeyer et al, 2001). |
| References |
Kuo ML, Lee KC, Lin JK. (1992) Genotoxicities of nitropyrenes and their modulation by Apigenin, tannic acid, ellagic acid and indole-3-carbinol in the Salmonella and CHO systems. Mutat. Res. 270(2):8-95 PMID 1383740 Lee SF, Lin JK (1997) Inhibitory effects of phytopolyphenols on TPA-induced transformation, PKC activation, and c-jun expression in mouse fibroblast cells. Nutr Cancer 28:177–183 PMID 9290125 Lindenmeyer F, Li H, Menashi S, Soria C, Lu H (2001) Apigenin acts on the tumor cell invasion process and regulates protease production. Nutr. Cancer. 2001;39:139–147 PMID 11588896 Middleton E Jr, Kandaswami C, Theoharides TC (2000) The effects of plant flavonoids on mammalian cells: Implications for inflammation, heart disease, and cancer. Pharmacol. Rev. 52(4):673-751 PMID 8895505 Plaumann B, Fritsche M, Rimpler H, Brandner G, Hess RD (year) . Flavonoids activate wild-type p53. Oncogene. 1996;13:1605–1614 PMID 8895505 Shukla S and Gupta S (2010) Apigenin: A promising molecule for cancer prevention. Pharm. Res. 27(6): 962-978 PMID 20306120 Yang CS, Landau JM, Huang MT, Newmark HL (2001) Inhibition of carcinogenesis by dietary polyphenolic compounds. Annu Rev. Nutr. 21:381-406 PMID 11375442 |
