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Hepatocellular carcinoma (HCC) is one of the most common causes of death from cancer worldwide. The poor prognosis of HCC is due to high recurrence rate mainly caused by intrahepatic metastasis. Paxillin was known to be a central adaptor protein for mediating focal adhesion (FA) signal required for HCC progression. However, target therapy aiming at paxillin seems unfeasible due to its ubiquitous tissue expression and essential biological functions. Within the paxillin superfamily, hydrogen peroxide inducible clone-5 (Hic-5) is the most homologous to paxillin. This review summarises the recent findings relevant to the differential biochemical and biological roles of Hic-5 and paxillin. Given the structure similarity between Hic-5 and paxillin, Hic-5 shares many of the characteristics of paxillin, including the localization of Hic-5 at focal adhesions and similar FA binding factors.  However, some of the regulatory mechanisms and molecular functions of Hic-5 are rather different from those of paxillin. These might explain the differential roles of both adaptors in regulating various pathophysiological processes. Interestingly, both adaptors might play distinct but complementary roles in tumor progression. Due to the more limited tissue distribution of Hic-5, it can be a more suitable therapeutic target for preventing HCC progression.