Apigenin is a bioactive flavonoid with anti-inflammatory, antioxidant and anticancer properties which is found in common fruits and vegetables.
In epidemiologic studies, a diet rich in flavones has possibly been shown to be related to a decreased risk of breast, digestive tract, skin, prostate and certain hematological cancers.
Most of the benefits are related to apoptosis – normal, programmed cell death which is part of the natural renewal and replacement of cells in our body. We want to encourage apoptosis in cancer cells.
In relation to prostate cancer the following has been found:
Androgen-independent human prostate cancer PC-3 cells show complete growth retardation after apigenin exposure. Source: [Source]
Long term treatment of human prostate carcinoma cells with low concentrations of quercetin, apigenin and kaempferol induced a process called tyrosine dephosphorylation. This in turn inactivated an cancer causing substance called PDPK FA. [Source].
Apigenin has the capability to significantly reduce cell number and induce cell death in the following cancer cell types:
The PC-3 and DU145 cells were less susceptible to apigenin induced cell death than LNCaP and PWR-1E cells. This was dependent on caspases which are chemicals found in cells and which have a role in apoptosis.
In cancer cells Apigenin has a positive role in the following processes:
- Generates a type of free radical called reactive oxygen species. Elevated levels of this are found in all cancer types yet they are implicated in cancer cell death. [Source]
- Reduces expression of mitochondrial Bcl-2. This is an anti-apoptotic protein and its over-expression in LNCaP B10 cells reduces the positive effects of apigenin. [Source]
- Increases mitochondrial permeability in cancer cells, which generally precedes cell death. [Source]
- Causes cytochrome C release which is an important factor in cell death. [Source]
- Induces cleavage of caspase 3, 7, 8, and 9. Caspase is an important factor in cell death and cleavage is part of the process of activating them. [Source]
Apigenin treatment to NHPE and PZ-HPV-7 resulted in growth inhibitory responses of low magnitude but significant decrease in cell viability was observed in CA-HPV-10 cells. [Source]
But most importantly…
A major benefit of Apigenin is that it helps to achieve a significant decrease in Androgen Receptor (AR) protein expression. In so doing it decreases sensitivity to androgens. In some cancers increased AR expression can make cells more sensitive to androgens even when they are relatively absent. Anyone going through Androgen Deprivation Therapy will understand and appreciate the possible role of Apigenin in improving and extending the effectiveness of this treatment
The inhibitory effects of apigenin on androgen-refractory human prostate carcinoma DU145 cells were studied. These types of cell no longer respond to Androgen Deprivation Therapy and have mutations in the tumor suppressor gene p53 and pRb. Exposure of DU145 cells to Apigenin resulted in inhibition of growth and colony formation as well as interruption of the cell cycle.
Apigenin exposure also resulted in alteration in Bax/Bcl2 ratio in favor of apoptosis, which was associated with the release of cytochrome c and induction of apoptotic protease-activating factor-1 (Apaf-1). This effect was found to result in a significant increase in cleaved fragments of caspase-9, -3, and poly (ADP-ribose) polymerase (PARP).
Exposure of PC-3 cells to apigenin inhibited DNA binding and reduced nuclear levels of the p65 and p50 subunits of NF-κB with concomitant decrease in IκBα degradation, IκB-α phosphorylation and IKKα kinase activity.