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5th World Congress on Cancer Therapy

Atlanta, USA

Swei Sunny Hann

The Second Clinical Medical Collage, University of Guangzhou Traditional Chinese Medicine, China

Title: Baicalein increases the expression and reciprocal interplay of RUNX3 and FOXO3a through crosstalk of AMPKa and ERK1/2 signaling pathways in human non-small cell lung cancer cells


Biography: Swei Sunny Hann


Baicalein, a natural fl avonoid obtained from the Scutellaria baicalensis root, has been reported to inhibit growth of human lung cancer. However, the detailed mechanism underlying this eff ect has not been well elucidated. We showed that baicalein signifi cantly inhibited the growth and induced apoptosis of NSCLC in a time- and dose-dependent manner. Baicalein induced RUNX3 and FOXO3a mRNA and protein expression, and increased phosphorylation of AMPK and ERK1/2. Moreover, the inhibitors of AMPK and ERK1/2 reversed the eff ect of baicalein on RUNX3 and FOXO3a protein expression. Interestingly, while compound C had little eff ect on blockade of baicalein-induced phosphorylation of ERK1/2, PD98059 signifi cantly abrogated the baicalein-induced phosphorylation of AMPK. Intriguingly, while silencing of RUNX3 abolished the eff ect of baicalein on expression of FOXO3a and apoptosis, silencing of FOXO3a signifi cantly attenuated baicalein-reduced cell proliferation. On the contrary, overexpression of FOXO3a restored the eff ect of baicalein on cell growth inhibition in cells silencing of endogenous FOXO3a gene and enhanced the eff ect of baicalein on RUNX3 protein expression. Finally, exogenous expression of RUNX3 increased FOXO3a protein and strengthened baicalein-induced phosphorylation of ERK1/2 and. Collectively, our results show that baicalein inhibits growth and induces apoptosis of NSCLC cells through AMPKα- and ERK1/2-mediated increase and interaction of FOXO3a and RUNX3. Th e crosstalk between AMPK and ERK1/2 signaling pathways, and the reciprocal interplay of FOXO3a and RUNX3 converge on the overall response of baicalein. Th is study reveals a novel mechanism for regulating FOXO3a and RUNX3 signaling axis in response to baicalein and suggests a new strategy for NSCLC associated targeted therapy.