Black Cumin and Cancer

[Guest guest]

UNIQUE ID: 98638377

 

AUTHOR: Medenica R, Janssens J, Tarasenko A, Lazovic G, Corbitt W,

Powell D, Jocic D, Mujovic V

 

ADDRESS: International Immuno-Biology Research Laboratory, South

Carolina, 29926

 

TITLE: Anti-angiogenic activity of nigella sativa plant extract in

cancer therapy (Meeting abstract).

 

SOURCE: Proc Annu Meet Am Assoc Cancer Res; 38:A1377 1997

 

ABSTRACT:

 

Nigella sativa [NS], or 'black cumin', an annual herb belonging to the

family Ranunculaceae, has strong immunomodulatory and interferon like

activity. We confirm that our extract of NS inhibits cancer and

endothelial cell progression, decreases the production of the angiogenic

protein-fibroblastic growth factor (FGF) made by tumor cells, and

inhibits growth factor for endothelial cells. FGF-1 and FGF-2 are both

localized to myoepithelial and to epithelial cells. FGF is an autocrine

growth factor developed in our immortalized human mammary epithelial

cells.

 

FGF-2, present in aggressive breast cancer, was suppressed by NS. In

addition, our breast cancer cell line contains FGF 1-4. Tumor growth is

angiogenesis dependent and neo-vascularization is a crucial determinant

of the metastatic potential of the tumor. Formed vessels in tumors are

hyper permeable to plasma protein, due to gaps in the endothelial

lining. These vascular abnormalities could facilitate entry of the tumor

cells into the circulation. We studied breast cancer, prostate cancer

and melanoma cells for acidic fibroblast growth factor which we isolated

and suppressed by NS. We attempted to recapitulate early angiogenic

evidence in vitro by developing a model of endothelial growth migration

and extra cellular matrix interaction. Our in vitro assay revealed that

stimulated endothelial cells can produce degradative proteinase and

invade the extra cellular matrix similarly to tumor cells.

 

Moreover, this model system indicated that a fine tuned balance between

proteinase and proteinase inhibitor regulates vascular morphogenesis and

invasion. Migrating endothelial cells produce Type 4 collagenase (member

of the matrix metalloproteinase family) and serineproteinase.

 

We demonstrated that specific inhibitors of Type 4 collagenase, general

metalloproteinase inhibitors and serineproteinase inhibitors blocked

endothelial cell invasion of the extra cellular matrix. These inhibitors

blocked tumor cell invasion in the same assay. NS was compared with

these factors and shown to have the same action. The endothelial cells

in culture were reverted to a non-angiogenic state when the angiogenic

stimulus is neutralized by NS. The activity of NS blocked the tumor

growth and dissemination in metastasis and have remarkable promises for

clinical use.