title: Ginkgo may prevent genetic-associated ovarian cancer risk:  multiple biomarkers and anticancer pathways induced by ginkgolide B in BRCA1-mutant ovarian epithelial cells.
abstract: Women carrying BRCA1 mutations have a higher risk of developing ovarian cancers. Options to reduce this risk are largely limited to prophylactic surgery, which leads to a decrease in the quality of life and permanently damages fertility. There is a obvious and an urgent need to identify a noninvasive approach to effectively prevent the ovarian cancer risk, specifically for those women of reproductive age. Our previous studies showed that the use of the herbal remedy Ginkgo biloba may reduce the risk for nonmucinous ovarian cancer. Here, we explored whether Ginkgo biloba might also be an effective agent to reduce BRCA1-associated ovarian cancer (always serous-type) risk. A human ovarian surface epithelial cell line-636 was developed from a BRCA1-mutant carrier. Cells were treated with ginkgolide B (GB) or dimethyl sulfoxide, and protein lysates from the cells were applied to antibody microarrays to determine upregulated or downregulated protein expression patterns. Anticancer activities and the associated networking pathways with the altered proteins were analyzed by using the Pathway Studio software. After GB treatment, 28 proteins were shown to be consistently upregulated (1.5-15.5-fold), and 22 proteins were downregulated (1.5-28.3-fold). Bioinformatics software analysis indicated that multiple mechanisms and signal pathways are involved in anticancer activities in BRCA1-mutant cells induced by GB treatment. These pathways include cell proliferation, tumor suppression, and DNA damage repair. Our study suggested that GB found in the herbal Ginkgo biloba may have cancer-preventive activities in BRCA1-mutant ovarian epithelial cells.
authors.affiliation: Obstetrics and Gynecology Hospital, Department of Obstetrics and Gynecology of Shanghai Medical School, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Jiang
authors.forename: Weiliang
authors.initials: W
authors.lastname: Qiu
authors.forename: Yisheng
authors.initials: Y
authors.lastname: Wang
authors.forename: Qing
authors.initials: Q
authors.lastname: Cong
authors.forename: Dale
authors.initials: D
authors.lastname: Edwards
authors.forename: Bin
authors.initials: B
authors.lastname: Ye
authors.forename: Congjian
authors.initials: C
authors.lastname: Xu
mesh_terms: D002461:Cell Line, Transformed; D049109:Cell Proliferation / Q000187:drug effects; D004249:DNA Damage / Q000187:drug effects / Q000235:genetics; D004847:Epithelial Cells / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D005260:Female; D019398:Genes, BRCA1 / Q000502:physiology*; D005819:Genetic Markers / Q000235:genetics*; D046934:Ginkgolides / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D007783:Lactones / Q000494:pharmacology* / Q000627:therapeutic use; D009154:Mutation / Q000235:genetics*; D010051:Ovarian Neoplasms / Q000188:drug therapy / Q000235:genetics*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology
chemical_list: D005819:Genetic Markers; D046934:Ginkgolides; D007783:Lactones; C045856:ginkgolide B