AF1q enhancement of gamma irradiation-induced apoptosis by up-regulation of BAD expression via NF-kappa B in human squamous carcinoma A431 cells
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AbstractBAD (BCL-2 antagonist of cell death) is a proapoptotic BCL-2 family protein that plays a critical role in the regulation of apoptotic response. This study presents direct evidence that AF1q increased the radiation-induced apoptosis through up-regulation of BAD in human squamous carcinoma A431 cells and the key transcription factor involved is NF-kappa B. The minimal promoter sequence of BAD was identified; the activity was increased in AF1q stable transfectants and decreased upon AF1q siRNA transfection. The NF-kappa B consensus binding sequence is detected on BAD promoter. Inactivation of NF-kappa B by NF-kappa B inhibitor Bay 11-7082 or NF-kappa B p65 siRNA suppressed the expression and promoter activity of BAD; the suppression is more obvious in AF1q stable transfectants which also have an elevated NF-kappa B level. Mutation of putative NF-kappa B motif decreased the BAD promoter activity. The binding of NF-kappa B to the BAD promoter was confirmed by chromatin-immunoprecipitation. These findings indicate that AF1q up-regulation of BAD is through its effect on NF-kappa B and this may hint of its oncogenic mechanism in cancer.
All Author(s) ListCo NN, Tsang WP, Tsang TY, Yeung CLA, Yau PL, Kong SK, Kwok TT
Journal nameOncology Reports
Volume Number24
Issue Number2
Pages547 - 554
LanguagesEnglish-United Kingdom
Keywordsapoptosis; gamma irradiation; NF-kappa B; squamous carcinoma
Web of Science Subject CategoriesOncology; ONCOLOGY

Last updated on 2021-13-09 at 23:51