Effects of the Bowman-Birk inhibitor on clonogenic survival and cisplatin- or radiation-induced cytotoxicity in human breast, cervical, and head and neck cancer cells

• Published in: Nutrition and cancer Vol. 33; no. 2; pp. 165 - 173
• Main Authors: Zhang, L, Wan, X.S, Donahue, J.J, Ware, J.H, Kennedy, A.R
• Format: Journal Article
• Language: English
• Published: United States Lawrence Erlbaum Associates, Inc 01.01.1999
• Subjects: Adenocarcinoma - pathology; Analysis of Variance; bowman-birk inhibitor concentrte; breast neoplasms; Breast Neoplasms - pathology; carcinogens; carcinoma; Carcinoma, Squamous Cell - pathology; cell killing; cell lines; cervix; Cisplatin; concentrates; cytotoxicity; dose response; Dose-Response Relationship, Drug; epithelium; Female; head; Head and Neck Neoplasms - pathology; Humans; malignant course; mortality; neck; neoplasms; proteinase inhibitors; Radiation; Trypsin Inhibitor, Bowman-Birk Soybean - pharmacology; Trypsin Inhibitors - pharmacology; Tumor Cells, Cultured - drug effects; Tumor Stem Cell Assay; Uterine Cervical Neoplasms - pathology
• ISSN: 0163-5581; 1532-7914
• DOI: 10.1207/S15327914NC330208

Bowman-Birk inhibitor (BBI) is a soybean-derived anticarcinogenic protease inhibitor previously shown to potentiate cisplatin-induced cytoxicity in human lung and ovarian cancer cells. To further assess the potential of BBI as a sensitizing agent for cancer radiotherapy and chemotherapy, we evaluated the effects of BBI and a soybean concentrate enriched in BBI known as BBI concentrate (BBIC) on clonogenic survival and radiation- or cisplatin-induced cell killing in MCF7 human breast carcinoma cells, SCC61 and SQ20B human head and neck carcinoma cells, HeLa, HeLa-R1, and HeLa-R3 human cervical carcinoma cells, MCF10 nontumorigenic human epithelial cells, HTori-3 nontumorigenic human thyroid epithelial cells, and C3H10T1/2 mouse fibroblast cells. BBI and BBIC significantly suppressed the clonogenic survival of MCF7 and SCC61 cells. BBIC also suppressed the survival of SQ20B cells and enhanced radiation-induced cell killing in SCC61 and SQ20B cells and cisplatin-induced cell killing in HeLa, HeLa-R1, and HeLa-R3 cells. In contrast, BBI and/or BBIC did not enhance radiation-induced cell killing in MCF10 cells or cisplatin-induced cell killing in C3H10T1/2 cells. BBI did not significantly affect the survival of SQ20B cells or enhance radiation-induced cell killing in SCC61 and SQ20B cells. The clonogenic survivals of MCF10 and C3H10T1/2 cells were not adversely affected by treatment with BBI or BBIC. The clonogenic survival of HTori-3 cells was only moderately suppressed by treatment with BBIC at > or = 80 micrograms/ml. These results suggest that BBIC could be a use agent for the potentiation of radiation- and cisplatin-mediated cancer treatment without significant adverse effects on surrounding normal tissues.