Journal
INVESTIGATIONAL NEW DRUGS
Volume 29, Issue 2, Pages 273-284Publisher
SPRINGER
DOI: 10.1007/s10637-009-9359-9
Keywords
Azoxymethane; Luteolin; Colon cancer; PCNA; beta-catenin; Cyclin D1; Cell proliferation
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Funding
- Council of Scientific and Industrial Research (CSIR), New Delhi, India
- Council of Scientific and Industrial Research (CSIR), PAK
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The protective role of Luteolin (LUT) against Azoxymethane (AOM)-induced mouse colon carcinogenesis has been documented earlier. The aim of this study is to investigate on the mechanism of chemopreventive action exhibited by LUT employing AOM-induced colon carcinogenesis in mice as an experimental model. LUT inhibited AOM-induced colon tumorigenesis by decreasing tumor incidence and size. LUT reduced the cell proliferation by decreasing the number of Argyrophillic nucleolar organizer region (AgNOR)/nucleus and Proliferating Cell Nuclear Antigen (PCNA) index. It was known that beta-catenin is a key effector in Wingless and Int (Wnt) signaling pathway and 90% of colon tumors arise from mutations in this pathway. In this study, we show evidence that LUT inhibited colon carcinogenesis by decreasing AOM-induced cell proliferation through the involvement of beta-catenin, Glycogen synthase kinase (GSK)-3 beta and cyclin D1, the key components in Wnt signaling pathway. In conclusion, the protective effect of LUT could be attributed to inhibition of AOM-induced cellular proliferation probably through the involvement of beta-catenin, GSK-3 beta and cyclin D1.
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