| Summary: | 碩士 === 國立清華大學 === 分子與細胞生物研究所 === 102 === Abstract
PTEN is a tumor suppressor protein that inhibits cell growth and viability by modulating the PI3K/AKT signaling pathway. Zinc has been reported to cause PTEN degradation in the airway epithelium. In this study, we further investigate how zinc impact on the PTEN protein and bioeffect in BEAS-2B cells. First, we showed that zinc can suppress the level of PTEN. In previous studies, Reportedly, K13 and K289 are two major monoubiquitination sites that related to PTEN stability. We expressed PTENK13/K289E mutant into BEAS-2B cells and found that BEAS-2B cell was still sensitive to Zinc treatment. Noticeably, zinc activates IKK activity and reduces IκB level in the cells. Administration of Akt inhibitor did not block the zinc-induced IKK activation. Finally, we also examined whether cell viability is associated with the zinc-induced PTEN degradation. The result shows that zinc induce BEAS-2B cell death which is not related to apoptosis, necrosis or autophagy. There is increasing evidence showing that zinc plays a key role in many signaling pathway. However, the underlying mechanisms are poorly understood. Here we assessed the effect of zinc on PTEN and NFκB through a non apoptotic cell death, and the detailed mechanisms needs further investigation.
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