Abstract Title:

Luteolin inhibits cell proliferation during Azoxymethane-induced experimental colon carcinogenesis via Wnt/β-catenin pathway.

Abstract Source:

Invest New Drugs. 2009 Dec 15. Epub 2009 Dec 15. PMID: 20013030

Abstract Author(s):

Pandurangan Ashokkumar, Ganapasam Sudhandiran

Article Affiliation:

Department of Biochemistry, University of Madras, Guindy campus, Chennai, 600 025, Tamil Nadu, India.


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)-3beta 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-3beta and cyclin D1.

Study Type : In Vitro Study
Additional Links
Pharmacological Actions : Antiproliferative : CK(6801) : AC(5032)

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