Modulating effect of Enicostemma littorale on the expression pattern of apoptotic, cell proliferative, inflammatory and angiogenic markers During 7, 12-Dimethylbenz (a) anthracene induced hamster buccal pouch carcinogenesis

Abstract

Enicostemma littorale leaves are traditionally used for the treatment of several diseases, including inflammation and cancer. This study has taken effort to explore the antitumor initiating potential of E. littorale leaves (ElELet) by analyzing the expression pattern of apoptotic (p53, Bcl-2 and Bcl-2 associated X-protein), cell-proliferative (cyclin D1 and proliferating cell nuclear antigen), angiogenic (vascular endothelial growth factor), invasive (matrix metalloproteinase-2 and 9), and inflammatory (NF-κB and cyclooxygenase-2) markers during 7, 12-dimethylbenz (a) anthracene (DMBA) induced hamster buccal pouch carcinogenesis. Oral tumors were induced in the buccal pouches of hamsters using the potent site and organ specific carcinogen, DMBA. DMBA application 3 times a week for 14 weeks resulted in tumor formation in the buccal pouches. Hundred percent tumor formations with dysregulation in the expression pattern of apoptotic, cell proliferative, inflammatory, angiogenic, and invasive markers were observed in the buccal pouches of hamsters treated with DMBA alone. ElELet at a dose of 250 mg/kg body weight orally to DMBA treated hamsters significantly prevented the tumor formation as well as corrected the abnormalities in the expression pattern of above mentioned molecular markers. ElELet thus modulated the expression pattern of all the above mentioned molecular markers in favor of the suppression of cell proliferation occurring in DMBA induced hamster buccal pouch carcinogenesis.

Efficacy of Hydroxytyrosol as Chemopreventive Agent on Induced Hamster Buccal Pouch Carcinogenesis

“…These results are in agreement with those of other studies (12,14,15,39) . The increased level of Bcl-2 expression indicated that, inhibition of apoptosis by prevention the release of cytochrome C from mitochondria and promotion of carcinogenesis, While the decreased expression of Bak could be due to reduced apoptotic cell death as well as accelerated their growth (32,40) .…”

Emodin Efficacy on the Akt, Mapk, Erk and DNMT Expression Pattern During Dmba-Induced Oral Carcinoma in Golden Syrian Hamsters

“…Oral cancer arises due to the abnormalities in multiple molecular pathways, which include pathways of cell proliferation, apoptosis, inflammation and angiogenesis (Manoharan et al, 2015). Extensive studies utilized these molecular pathways to evaluate the antitumor potential of the medicinal plants, their active constituents and synthetic agents (Schetter et al, 2010).…”

Effect of crude latex from Euphorbia tirucalli on DMBA-induced carcinogenesis

“…The development of cancer is a multistep process with three distinct phases: initiation, promotion and progression [24]. The carcinogen DMBA is a chemical initiator and promoter of carcinoma in the oral mucosa [25] through production of free radicals (byproducts of its metabolism), leading to the damage of DNA, cell membranes and proteins as well as the dysregulation of anti-apoptotic mediators [26,27]. After the topical application of 0.5% DMBA in acetone for a period of 20 weeks, histopathological alterations similar to cancerous lesions in humans are found on the oral mucosa [25].…”