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Title 

Dysregulation of overexpressed IL-32alpha in hepatocellular carcinoma suppresses cell growth and induces apoptosis through inactivation of NF-kappaB and Bcl-2

Authors 

Yun Hee KangM Y ParkD Y YoonS R HanC I LeeN Y JiP K MyungHee Gu LeeJae Wha KimYoung Il YeomYe Jin JangD K AhnJ W KimEun Young Song

Publisher 

Elsevier

Issue Date 

2012

Citation 

Cancer Letters, vol. 318, no. 2, pp. 226-233

Keywords 

ApoptosisCell growthDiagnostic markerHepatocellular carcinomaIL-32α

Abstract 

IL-32 is a newly discovered cytokine. Recently, various reports suggest that it plays a role as a proinflammatory mediator and may be involved in several cancer carcinogenesis. However, IL-32 expression in hepatocellular carcinoma (HCC) remains unclear. In this study, we investigated the expression and role of IL-32α in hepatocellular carcinoma, because IL-32 was identified as an upregulated gene in hepatocellular carcinoma tissues compared to nontumorous regions using DNA microarray. IL-32α was overexpressed in tissue and serum from patients with HCC and localized in the cytoplasm and nucleus of hepatocellular carcinoma tumor cells. Moreover, secreted IL-32α concentration in the serum of patients with hepatocellular carcinoma was elevated as compared with those in the normal serum using a developed sandwich ELISA. Furthermore, IL-32α suppression in hepatocellular carcinoma decreased expression of phospho-p38 MAPK, NF-κB, and antiapoptotic protein Bcl-2 and induced expression of proapoptotic proteins as well as p53 and PUMA resulting in the suppression of cell growth and induction of intrinsic apoptosis. Based on our results, we suggest that IL-32α is involved in the progression of hepatocellular carcinoma and may be a useful biomarker for diagnosis and therapeutic target of hepatocellular carcinoma.

ISSN 

0304-3835

Link 

http://dx.doi.org/10.1016/j.canlet.2011.12.023

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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