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http://dx.doi.org/10.5352/JLS.2007.17.9.1298

(β-lapachone Regulates Tight Junction Proteins, Claudin-3 and -4, in Human Hepatocarcinoma Cells.  

Kim, Sung-Ok (Department of Biomaterial Control (BK21 Program), Dongeui University Graduate School)
Kwon, Jae-Im (Department of Biochemistry, Dongeui University Graduate School)
Kim, Gi-Young (Faculty of Applied Marine Science, Cheju National University)
Kim, Nam-Deuk (Division of Pharmacy (BK21 Program), Pusan National University)
Choi, Yung-Hyun (Department of Biomaterial Control (BK21 Program), Department of Biochemistry, Dongeui University Graduate School)
Publication Information
Journal of Life Science / v.17, no.9, 2007 , pp. 1298-1302 More about this Journal
Abstract
A hallmark of cancers is 'leaky' tight junctions (Tjs). TJs mediated paracellular permeability is elevated and TJs maintained cell polarity is frequently lost. Concomitantly, TJs-associated proteins including members of the claudin family of proteins are dysregulated. Recent findings indicate that these TJs changes can contribute to cancer progression. In this study, we examined the effects of ${\beta}-lapachone$, a quinone compound obtained from the bark of the lapacho tree (Tabebuia avellanedae), on the Tjs-associated regulators in human hepatocarcinoma cell lines, HepG2 and Hep3B. ${\beta}-lapachone$ treatment downregulated the levels of insulin-like growth factor 1 receptor (IGF-lR) proteins in both HepG2 and Hep3B cells. But the levels of claudin-3 and -4 proteins were increased in ${\beta}-lapachone$-treated HepG2 and Hep3B cells. And also the zonnula occludens-l (la-I) and p-catenin protein levels by ${\beta}-lapachone$ were increased in a time-dependent manner. However, claudin-3 and -4 mRNA levels were uninhibited by ${\beta}-lapachone$ in HepG2 and Hep3B. The present results suggest that the upregulation of claudin-3 and -4 protein levels by ${\beta}-lapachone$ occurs by a post-transcriptional mechanism and points to a novel mechanism by ${\beta}-lapachone$.
Keywords
${\beta}-lapachone$; tight junction; IGF-1R; claudins; ZO-1; ${\beta}-catenin$;
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