Use of Ginkgo extract
View Patent ↗The present invention is directed to the use of the extract of Ginkgo biloba leaves or isolated Ginkgolide B (GKB), a component of the extract of Ginkgo biloba leaves in a method for decreasing the expression of peripheral-type benzodiazepine receptor (PBR) in cells of a patient in need thereof. Further, the present invention is directed to the use of the extract of Ginkgo biloba leaves or isolated GKB in a method for decreasing the proliferation of cancer cells in a patient. More particularly, the present invention is directed to the use of the extract of Ginkgo biloba leaves or isolated GKB in a method of decreasing cancer cell proliferation in a patient wherein the cancer cell is human breast cancer cell. Even more particularly, the present invention is directed to the use of the extract of Ginkgo biloba leaves or isolated GKB in method of decreasing cancer cell proliferation in a patient wherein the cancer cell is of the aggressive and invasive phenotype and expresses high levels of PBR in comparison to non-aggressive cancer cell.
1. A method of inhibiting the proliferation of breast cancer cells in a patient in need of such inhibition, wherein said breast cancer cells are characterized by increased expression of peripheral-type benzodiazepine receptor protein, which comprises:
determining whether said breast cancer cells exhibit elevated expression of peripheral-type benzodiazepine receptor protein, wherein said elevated expression is an at least 3-fold increase in the level of expression of peripheral-type benzodiazepine receptor protein as compared to normal cells; and
administering an effective amount of isolated Ginkgolide B to said patient.
2. A method according to claim 1 , wherein said proliferation of breast cancer cells is caused by the over-expression of oncogenes, and wherein the administering results in decreasing the expression of said oncogenes and combats the proliferation of said breast cancer cells.
3. A method according to claim 2 , wherein said oncogenes are one or more of APC, PE-1, RhoA and c-Jun.
4. A method according to claim 1 , wherein said administering results in decreasing the expression of peripheral-type benzodiazepine receptor in said breast cancer cells.
5. A method according to claim 4 , wherein said breast cancer cells are human breast cancer cells.
6. A method according to claim 4 , wherein the decreasing of the expression of peripheral-type benzodiazepine receptor is the result of decreasing the expression of peripheral-type benzodiazepine receptor mRNA in said breast cancer cells.
7. A method according to claim 1 , wherein said administering results in increasing the expression of a c-Myc protooncogene.
8. A method according to claim 1 , wherein said administering results in decreasing the expression of cell cycle regulators prothymosin-α, CDK2, p55CDC, myeloblastin and p120 proliferating-cell nuclear antigen.
9. A method according to claim 1 , wherein said administering results in decreasing the expression of intracellular signal transduction modulators NET1 and ERK2.
10. A method according to claim 1 , wherein said administering results in decreasing the expression of apoptosis-related products Adenosine A2A Receptor, Flt3 ligand, Grb2, Clusterin, RXR-β, Glutathione S-transferase P, N-Myc, TRADD, SGP-2 and NIP-1.
11. A method according to claim 1 , wherein said administering results in decreasing the expression of transcription factors Id-2, ATF-4, ETR101 and ETR-103.
12. A method according to claim 1 , wherein said administering results in decreasing the expression of growth factors macrophage colony-stimulating factor-1, heparin-binding EGF-like growth factor, hepatocyte growth factor-like protein and inhibin α.
13. A method according to claim 1 , wherein said administering results in decreasing the expression of cell adhesion molecules CD19 B-lymphocyte antigen, L1CAM, β-catenin, integrin subunits α3, α4, α6, β5, and αM.
14. A method according to claim 1 , wherein said administering results in decreasing the expression of genes APC, PE-1, RhoA, c-Jun, prothymosin-α, CDK2, p55CDC, myeloblastin, p120 proliferating-cell nuclear antigen, NET1, ERK2, Adenosine A2A Receptor, Flt3 ligand, Grb2, Clusterin, RXR-β, Glutathione S-transferase P, N-Myc, TRADD, SGP-2, NIP-1, Id-2, ATF-4, ETR-101, ETR-103, macrophage colony-stimulating factor-1, heparin-binding EGF-like growth factor, hepatocyte growth factor-like protein, inhibin α, CD19 B-lymphocyte antigen, L1CAM, β-catenin, and integrin subunits α3, α4, α6, β5, and αM.