Inhibitory effect of black tea on the growth of established skin tumors in mice: effects on tumor size, apoptosis, mitosis and bromodeoxyuridine incorporation into DNA

Abstract

Female CD-1 mice were initiated with a single topical application of 7,12-dimethylbenz[a]anthracene and promoted with 12-O-tetradecanoylphorbol-13-acetate. Mice with established papillomas were then treated with black tea or decaffeinated black tea (approximately 4 mg tea solids/ml) as the sole source of drinking fluid for 11-15 weeks. In four separate experiments, oral administration of black tea inhibited the growth of papillomas (increase in tumor volume/mouse) by an average of 35%, 37%, 41% and 48%, respectively. Studies with decaffeinated black tea gave inconsistent results. In one experiment, administration of decaffeinated black tea inhibited papilloma growth (increase in tumor volume/mouse) by 27%, but in two additional experiments papilloma growth was stimulated by 14% and 193%, respectively. In a separate experiment, skin tumors were generated by treating SKH-1 female mice with ultraviolet B light (UVB; 30 mJ/cm2) twice weekly for 22 weeks, after which UVB administration was stopped. Tumors were allowed to develop during the following 13 weeks, and tumor-bearing mice were then treated with black tea (6 mg/ml tea solids) as the drinking fluid for 11 weeks. In this experiment, tumor growth (increase in tumor volume/mouse) was inhibited by 70%. Histological examination revealed that tea-treated mice had a 58% decrease in the number of nonmalignant tumors (primarily keratoacanthomas)/mouse and a 54% decrease in the number of squamous cell carcinomas/mouse. In addition, administration of black tea decreased the volume per tumor by 60% for nonmalignant tumors and by 84% for carcinomas. Mechanistic studies with tumors from these mice revealed that administration of black tea decreased the bromodeoxyuridine labeling index in squamous cell papillomas, keratoacanthomas and squamous cell carcinomas by 56%, 45% and 35%, respectively, and the apoptosis index was increased by 44%, 100% and 95%, respectively. Administration of black tea decreased the mitotic index in keratoacanthomas and squamous cell carcinomas by 42% and 16%, respectively. The results indicate that oral administration of black tea to tumor-bearing mice inhibited proliferation and enhanced apoptosis in nonmalignant and malignant skin tumors.

Silibinin Protects against Photocarcinogenesis via Modulation of Cell Cycle Regulators, Mitogen-Activated Protein Kinases, and Akt Signaling

“…PCNA, a subunit of DNA polymerase, plays a crucial role in DNA replication and repair and serves as a biomarker of proliferation (22). Earlier studies have reported that inhibition of DNA synthesis and cell proliferation by black tea, green tea, caffeine, or epigallocatechin is associated with their cancer chemopreventive efficacy (7,23). Silibinin also inhibited UVB-induced DNA synthesis and cell proliferation, as observed by a decrease in BrdUrd incorporation and PCNA-positive cells in uninvolved skin and tumors, suggesting a plausible role of in vivo antiproliferative effect of silibinin in its overall efficacy against UVB-induced tumorigenesis.…”

Green Tea in Prevention and Therapy of Prostate Cancer

“…Recent laboratory studies have indicated that green tea and its polyphenolic constituents impart inhibitory effects on the activities of many enzymatic, metabolic and signaling pathways that have relevance to cancer development and progression (31)(32)(33)(34)(35)(36). A number of studies have shown the growth inhibitory effects of green tea against many animal tumor bioassay systems including lung, skin and forestomach (37)(38)(39)(40).…”

Health benefits of Green and Black Tea: A Review

“…Early studies have demonstrated that topical application or ingestion ofgreen tea polyphenols or EGCG inhibit tumor initiation and promotion by chemical carcinogens and UV light in mice [26]- [29]. Black tea has similar effects [29]- [32]. Topical application of a greentea polyphenolic fraction on mice skin papillomas can decrease significantly the conversion of benign tumors tomalignant tumors [33].…”