Paper
28 October 2009 PUMA promotes Bax translocation in FOXO3a-dependent pathway during STS-induced apoptosis
Yingjie Zhang, Qun Chen
Author Affiliations +
Abstract
PUMA (p53 up-regulated modulator of apoptosis, also called Bbc3) was first identified as a BH3-only Bcl-2 family protein that is transcriptionally up-regulated by p53 and activated upon p53-dependent apoptotic stimuli, such as treatment with DNA-damaging drugs or UV irradiation. Recently studies have been shown that Puma is also up-regulated in response to certain p53-independent apoptotic stimuli, such as growth factor deprivation or treatment with glucocorticoids or STS (staurosporine). However, the molecular mechanisms of PUMA up-regulation and how PUMA functions in response to p53-independent apoptotic stimuli remain poorly understood. In this study, based on real-time single cell analysis, flow cytometry and western blotting technique, we investigated the function of PUMA in living human lung adenocarcinoma cells (ASTC-a-1) after STS treatment. Our results show that FOXO3a was activated by STS stimulation and then translocated from cytosol to nucleus. The expression of PUMA was up-regulated via a FOXO3a-dependent manner after STS treatment, while p53 had little function in this process. Moreover, cell apoptosis and Bax translocation induced by STS were not blocked by Pifithrin-α (p53 inhibitor), which suggested that p53 was not involved in this signaling pathway. Taken together, these results indicate that PUMA promoted Bax translocation in a FOXO3a-dependment pathway during STS-induced apoptosis, while p53 was dispensable in this process.
© (2009) COPYRIGHT Society of Photo-Optical Instrumentation Engineers (SPIE). Downloading of the abstract is permitted for personal use only.
Yingjie Zhang and Qun Chen "PUMA promotes Bax translocation in FOXO3a-dependent pathway during STS-induced apoptosis", Proc. SPIE 7519, Eighth International Conference on Photonics and Imaging in Biology and Medicine (PIBM 2009), 75191A (28 October 2009); https://doi.org/10.1117/12.841118
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KEYWORDS
Cell death

Ultraviolet radiation

Proteins

Luminescence

Flow cytometry

Confocal microscopy

Lung

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