Abstract
Livin, a novel member of inhibitors of apoptosis protein, is highly expressed in tumor tissues. It is a potential target in tumor therapy. Silencing its gene expression has been found to promote tumor cell apoptosis or increase tumor sensitivity to therapies. This paper studied the effect of livin anti-apoptotic activity and examined its molecular mechanisms. In the study, higher levels of cell apoptosis were measured by FACS in the experiment group with livin expression silenced than that in controls (P < 0.05). After livin gene expression was knocked down, cleaved caspase-3 protein was up-regulated but caspase-3 mRNA expression was almost the same, the phosphorylated JNK1 protein was down-regulated but JNK1 mRNA and total JNK1 protein expression was approximately the same too. The results suggest that livin may exert anti-apoptotic action on SPC-A1 by activating JNK1 signaling pathway and inhibiting caspase-3 activation.




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Abbreviations
- RNAi:
-
RNA interference
- ShRNA:
-
Small hairpin RNA
- IAP:
-
Inhibitor of apoptosis protein
- BIR:
-
Baculoviral IAP repeats
- JNK1:
-
C-Jun N-terminal kinase 1
- p-JNK1:
-
Phosphorylated JNK1
- MOI:
-
Multiplicity of infection
- FACS:
-
Fluorescence activated cell sorting
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Acknowledgments
We thank Yaoqiong Cao, Jing Zheng (Gene Chem Co. Ltd, Shanghai, People’s Republic of China) for technical assistance. This study was supported by grants from the Natural Science Foundation of Fujian Province (No.: 2008J0074).
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Chen, YS., Li, HR., Lin, M. et al. Livin abrogates apoptosis of SPC-A1 cell by regulating JNKI signaling pathway. Mol Biol Rep 37, 2241–2247 (2010). https://doi.org/10.1007/s11033-009-9711-3
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DOI: https://doi.org/10.1007/s11033-009-9711-3