Lukasz
Jedi Master
I stumbled upon a book in which plant-derived substances with anti-cancer activity are summed up nicely, and it inspired me to start this thread. Some of the substances, like apigenin, seem to be especially interesting and I'll try to present them here. The book is only available in Polish - Roślinne terapie antynowotworowe w praktyce terapeutycznej by Lidia Wincek.
Apigenin
Apigenin blocks the development of cancer at various stages. It is considered to be one of the most active substances of the flavonoid group, which inhibits the multiplication of breast cancer cells.
Apigenin becomes particularly interesting in the case of hormonally dependent cancers. Research indicates that this compound may block estrogen receptors, which in turn results in the inhibition of cancer cell proliferation. Another mechanism, which has a beneficial effect on hormonal management in oncological patients, is blocking the aromatase enzyme that affects estrogen levels in the body.
Furthermore, studies have shown that apigenin:
Apigenin is found among others in camomile, celery leaves, parsley leaves, and St. John's wort.
There are various supplements and medications containing apigenin available on the market such as: capsules, tinctures and intravenous solutions. The dosage depends on the patient's weight and condition. The most common dose is about 100-150 mg of apigenin per day.
Related research:
Apigenin inhibits antiestrogen-resistant breast cancer cell growth through estrogen receptor-α-dependent and estrogen receptor-α-independent mechanisms
Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells (ARO)
Inhibition of aromatase activity by flavonoids
Apigenin Inhibits Growth of Breast Cancer Cells: The Role of ERα and HER2/neu
Apigenin inhibits pancreatic cancer cell proliferation through G2/M cell cycle arrest
Structure-activity relationships of flavonoids and the induction of granulocytic- or monocytic-differentiation in HL60 human myeloid leukemia cells
Flavones inhibit breast cancer proliferation through the Akt/FOXO3a signaling pathway
Apigenin induces apoptosis via extrinsic pathway, inducing p53 and inhibiting STAT3 and NFκB signaling in HER2-overexpressing breast cancer cells
Plant flavone apigenin inhibits HDAC and remodels chromatin to induce growth arrest and apoptosis in human prostate cancer cells: In vitro and in vivo study
Apigenin
Apigenin blocks the development of cancer at various stages. It is considered to be one of the most active substances of the flavonoid group, which inhibits the multiplication of breast cancer cells.
Apigenin becomes particularly interesting in the case of hormonally dependent cancers. Research indicates that this compound may block estrogen receptors, which in turn results in the inhibition of cancer cell proliferation. Another mechanism, which has a beneficial effect on hormonal management in oncological patients, is blocking the aromatase enzyme that affects estrogen levels in the body.
Furthermore, studies have shown that apigenin:
- inhibits the growth of leukemia cells
- plays an important role in the process of repair of DNA oxidative damage
- influences the inhibition of epidermal growth factor and tyrosine kinase, which confirms its anti-cancer and anti-metastatic properties
- has a beneficial effect on the gene of the tumor suppressor - p53 protein and inhibition of neoangiogenesis, i.e. formation of new blood vessels within the tumor
- has a strong antiproliferative function and ability to induce apoptosis of cancer cells
Apigenin is found among others in camomile, celery leaves, parsley leaves, and St. John's wort.
There are various supplements and medications containing apigenin available on the market such as: capsules, tinctures and intravenous solutions. The dosage depends on the patient's weight and condition. The most common dose is about 100-150 mg of apigenin per day.
Related research:
Apigenin inhibits antiestrogen-resistant breast cancer cell growth through estrogen receptor-α-dependent and estrogen receptor-α-independent mechanisms
An exciting aspect of this study is that apigenin has the potential to inhibit both ERα-dependent pathway and protein kinase–mediated growth factor signaling pathways. As both pathways are commonly altered in antiestrogen-resistant breast cancer, these broad effects of apigenin may be synergistic in combination with antiestrogens in growth inhibition of antiestrogen-resistant breast cancer cells.
Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells (ARO)
In summary, apigenin is a promising inhibitor of signal transduction pathways that regulate the growth (anchorage-dependent and independent) and survival of human anaplastic thyroid cancer cells. Apigenin may provide a new approach for the treatment of human anaplastic thyroid carcinoma for which no effective therapy is presently available.
Inhibition of aromatase activity by flavonoids
28 randomly selected flavonoids were screened for inhibitory effects against partially purified aromatase prepared from human placenta. Over 50% of the flavonoids significantly inhibited aromatase activity, with greatest activity being demonstrated with apigenin (IC50: 0.9 microg/mL), chrysin (IC50: 1.1 microg/mL), and hesperetin (IC50: 1.0 microg/mL).
Apigenin Inhibits Growth of Breast Cancer Cells: The Role of ERα and HER2/neu
It was shown that high doses of apigenin (50 μM) do not display estrogen-like activity and can suppress ER activation by 17β-estradiol.
Apigenin was found to be the most effective phytoestrogen that strongly inhibits the growth of breast cancer cells, including HER2-positive ones.
Apigenin inhibits pancreatic cancer cell proliferation through G2/M cell cycle arrest
Apigenin inhibits growth of pancreatic cancer cells through suppression of cyclin B-associated cdc2 activity and G2/M arrest, and may be a valuable drug for the treatment or prevention of pancreatic cancer.
Structure-activity relationships of flavonoids and the induction of granulocytic- or monocytic-differentiation in HL60 human myeloid leukemia cells
The flavones apigenin and luteolin strongly inhibited the growth of HL60 cells and induced morphological differentiation into granulocytes.
Flavones inhibit breast cancer proliferation through the Akt/FOXO3a signaling pathway
Data demonstrated that flavone, apigenin and luteolin induced cell cycle arrest and apoptosis in breast cancer cells through inhibiting PI3K/Akt activation and increasing FOXO3a activation, which suggest that flavone, apigenin and luteolin will be the potential leads for the preventing and treating of breast cancer.
Apigenin induces apoptosis via extrinsic pathway, inducing p53 and inhibiting STAT3 and NFκB signaling in HER2-overexpressing breast cancer cells
Our study indicates that apigenin could be a potential useful compound to prevent or treat HER2-overexpressing breast cancer.
Plant flavone apigenin inhibits HDAC and remodels chromatin to induce growth arrest and apoptosis in human prostate cancer cells: In vitro and in vivo study
Apigenin (4′,5,7,-trihydroxyflavone), an anticancer agent, selectively toxic to cancer cells induces cell cycle arrest and apoptosis through mechanisms that have not been fully elucidated. Our studies indicate that apigenin-mediated growth inhibitory responses are due to inhibition of class I histone deacetylases (HDACs) in prostate cancer cells.
Our findings confirm for the first time that apigenin inhibits class I HDACs, particularly HDAC1 and HDAC3 and its exposure results in reversal of aberrant epigenetic events that promote malignancy.