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Carcinogenesis, Vol. 24, No. 1, 75-80, January 2003
© 2003 Oxford University Press

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Apoptogenic effects of black tea on Ehrlich’s ascites carcinoma cell

Arindam Bhattacharyya, Tathagata Choudhuri, Suman Pal, Sreya Chattopadhyay, Goutam K. Datta, Gaurisankar Sa and Tanya Das1

Bose Institute, P-1/12 CIT Scheme VII M, Kolkata-700 054, India

Next to water, tea is the most ancient and widely consumed beverage in the world. Epidemiological studies have suggested a cancer protective effect, but the results obtained so far are not conclusive. In the current study, mechanisms of the apoptogenic effect of black tea extract were delineated. Black tea administration to Ehrlich’s ascites carcinoma (EAC)-bearing Swiss albino mice caused a significant decrease in the tumor cell count in a dose-dependent manner. Flowcytometric analysis showed an increase in the number of cells in the sub-G0/G1 population signifying tumor cell apoptosis by black tea. These results were further confirmed by nuclear staining that demonstrated distinct morphological features of apoptosis. Our data also revealed an increase in the expression of pro-apoptotic protein p53 in EAC. It is known that upon p53 induction, multiple downstream factors contribute to the decision making between growth arrest and apoptosis. Among those, pro-apoptotic gene Bax is up regulated during p53-mediated apoptosis. On the other hand, p53-mediated growth arrest involves p21 as a major effecter. In our system, increase in p53 expression was followed by moderate expression of p21/Waf-1 and high expression of Bax at protein levels. Interestingly, anti-apoptotic protein Bcl-2 was down regulated resulting in decrease in Bcl-2/Bax ratio. All these observations together signify that black tea-induced apoptogenic signals overrode the growth-arresting message of p21, thereby leading the tumor cells towards death.


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Correspondence re: M. Leone et al., Cancer Prevention by Tea Polyphenols Is Linked to Their Direct Inhibition of Antiapoptotic Bcl-2-Family Proteins. Cancer Res 2003;63:8118-21.
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