Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/40178
標題: HLJ1 is a novel caspase-3 substrate and its expression enhances UV-induced apoptosis in non-small cell lung carcinoma
作者: Lin, S.Y.
陳健尉
Hsueh, C.M.
Yu, S.L.
Su, C.C.
Shum, W.Y.
Yeh, K.C.
Chang, G.C.
Chen, J.J.W.
關鍵字: heat-shock-protein
radiation-induced apoptosis
stress-induced
apoptosis
cytochrome-c
tumor-suppressor
a549 cells
activation
cancer
death
survival
期刊/報告no:: Nucleic Acids Research, Volume 38, Issue 18, Page(s) 6148-6158.
摘要: Carcinogenesis is determined based on both cell proliferation and death rates. Recent studies demonstrate that heat shock proteins (HSPs) regulate apoptosis. HLJ1, a member of the DnaJ-like Hsp40 family, is a newly identified tumor suppressor protein closely related to relapse and survival in non-small cell lung cancer (NSCLC) patients. However, its role in apoptosis is currently unknown. In this study, NSCLC cell lines displaying varying HLJ1 expression levels were subjected to ultraviolet (UV) irradiation, followed by flow cytometry. Interestingly, the percentages of apoptotic cells in the seven cell lines examined were positively correlated with HLJ1 expression. Enforcing expression of HLJ1 in low-HLJ1 expressing highly invasive cells promoted UV-induced apoptosis through enhancing JNK and caspase-3 activation in NSCLC. Additionally, UV irradiation led to reduced levels of HLJ1 predominantly in apoptotic cells. The pan-caspase inhibitor, zVAD-fmk and caspase-3-specific inhibitor, DEVD-fmk, prevented UV-induced degradation of HLJ1 by the late stage of apoptosis. Further experiments revealed a non-typical caspase-3 cleavage site (MEID) at amino acid 125-128 of HLJ1. Our results collectively suggest that HLJ1 is a novel substrate of caspase-3 during the UV-induced apoptotic process.
URI: http://hdl.handle.net/11455/40178
ISSN: 0305-1048
文章連結: http://dx.doi.org/10.1093/nar/gkq412
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