Abstract
Apoptosis, also known as cell suicide or programmed cell death, removes unwanted and genetically damaged cells from the body. Evasion of apoptosis is one of the major characteristic features of rapidly proliferating tumor cells. Chemopreventive agents inhibit or suppress tumor formation through apoptotic induction in target tissues. The aim of the present study was to investigate the pro-apoptotic potential of lupeol during 7,12-dimethylbenz(a) anthracene (DMBA) induced hamster buccal pouch carcinogenesis. Topical application of 0.5% DMBA three times a week for 14 weeks in the buccal pouches of golden Syrian hamsters resulted in oral squamous cell carcinoma. The expression pattern of apoptotic markers was analyzed using immunohistochemistry (p53, Bcl-2, Bax) and ELISA reader (caspase 3 and 9). In the present study, 100% tumor formation with defects in apoptotic markerexpression pattern was noticed in hamsters treated with DMBA alone. Oral administration of lupeol at a dose of 50 mg/kg bw completely prevented the formation oral tumors as well as decreased the expression p53 and Bcl-2, while increasing the expression of Bax and the activities of caspase 3 and 9. The present study thus indicated that lupeol might inhibit DMBA-induced oral tumor formation through its pro-apoptotic potential in golden Syrian hamsters.
Highlights
Apoptosis, known as programmed cell death, plays an important role in the tissue homeostasis
100% tumor formation with defects in apoptotic markerexpression pattern was noticed in hamsters treated with dimethylbenz(a) anthracene (DMBA) alone
The present study demonstrates the modulating effect of lupeol on the expression pattern of apoptotic markers (p53, Bcl-2, Bax caspase 3 and 9) during DMBA-induced hamster buccal pouch carcinogenesis
Summary
Known as programmed cell death, plays an important role in the tissue homeostasis. P53, a putative regulator of multiple cellular processes, accumulates in response to DNA damage and oncogene activation. It can initiate apoptosis if DNA damage proves to be irreparable. Bcl-2, an anti-apoptotic protein, plays pivotal role in tumorigenesis and Bcl-2 inhibitors are currently under clinical trials for several malignancies (Chakravarti et al, 2012; Sun et al, 2012). Anti-apoptotic (Bcl-2) and pro-apoptotic proteins (Bax) determine the fate of damaged cells and imbalance in Bcl-2 to Bax ratio result in carcinogenesis (Gao et al, 2012). Caspase 3 and 9 have pivotal role in the process of programmed cell death. A large number of studies pointed out that caspases are deactivated during carcinogenesis (Kim et al, 2012 Song et al, 2012)
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