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Abstract: Poster Presentations |

HEME OXYGENASE-1 VIA TRANSCRIPTIONAL ACTIVATION OF NRF2 ATTENUATES APOPTOSIS IN A549 LUNG CANCER CELLS FREE TO VIEW

Euntaik Jeong, MD*; Hakryul Kim, MD; Seihoon Yang, MD
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Wonkwang University School of Medicine, Iksan, Jeonbuk, South Korea



Chest. 2006;130(4_MeetingAbstracts):234S-d-235S. doi:10.1378/chest.130.4_MeetingAbstracts.234S-d
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Abstract

PURPOSE: Heme oxygenase-1 (HO-1) is an inducible enzyme that catalyzes oxidative degradation of heme to form biliverdin, carbon monoxide, and free iron. Increasing evidences have indicated the critical role of HO-1 in cytoprotection and more diverse biological functions. HO-1 has been reported to stimulate tumor cell growth and proliferation. And several tumors, including renal cell carcinoma, prostate tumor, hepatocellular carcinoma, and sarcoma, express high level of HO-1.

METHODS: We previously demonstrated that HO-1 was expressed highly in A549 cells than other lung cancer cell lines. We aimed to investigate whether inhibition of HO-1 may induce apoptosis in A549 lung cancer cells.

RESULTS: ZnPP, specific HO inhibitor, significantly decreased the viability of A549 cells than other lung cancer cells in a dose-dependant fashion. Consistent with viability, HO enzymatic activity also decreased. Moreover, ZnPP induced the generation of intracellular H2O2 in a dose-dependent manner. A549 cells, next, were transfected by HO-1 small interfering RNA (siRNA) induced apoptosis, and Nrf2 siRNA resulted in decrease of HO-1 expression. However, NFkB siRNA had no influence on the expression of HO-1.

CONCLUSION: These findings suggest that increasing HO-1 expression in A549 cells may be resulted from the transcriptional activation of Nrf2, and inhibition of Nrf2-HO-1 pathway induces apoptosis.

CLINICAL IMPLICATIONS: Therefore it provides new important insights into the possible molecular mechanism of the antitumor therapy.

DISCLOSURE: Euntaik Jeong, None.

Wednesday, October 25, 2006

12:30 PM - 2:00 PM


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