Differential expression of Axl in hepatocellular carcinoma and correlation with tumor lymphatic metastasis.

Abstract:

:Protein kinases play important roles in tumor development and progression. A variety of members of the signal transduction enzymes serve as targets for therapeutic intervention in cancer. The dysregulation of Axl receptor and its ligand growth arrest-specific 6 (Gas6) is implicated in the pathogenesis of several cancers. In this study, the differential expressions of Axl were investigated in mouse hepatocarcinoma cell lines Hca-F and Hca-P, which have high- and low-metastatic potential to lymph nodes. Experimental inhibition of Axl by siRNA assessed further the metastatic potential of Axl. The results showed that down-regulation of Axl expression attenuated Hca-F cells proliferation, migration, and invasion in vitro, as well as inhibited metastasis to peripheral lymph nodes in vivo. Further analysis demonstrated that the addition of exogenous Gas6 mediated the migration and invasion of Hca-F cells both in vitro and in vivo through Axl. Furthermore, Gas6 stimulation of Axl in Hca-F cells resulted primarily in the down-regulation of Cyr61, a member of the CCN protein family involved in tumor progression. These data suggest that Axl acts as a tumor lymphatic metastasis-associated gene, and may function partly through the regulation of Cyr61.

journal_name

Mol Carcinog

journal_title

Molecular carcinogenesis

authors

He L,Zhang J,Jiang L,Jin C,Zhao Y,Yang G,Jia L

doi

10.1002/mc.20664

subject

Has Abstract

pub_date

2010-10-01 00:00:00

pages

882-91

issue

10

eissn

0899-1987

issn

1098-2744

journal_volume

49

pub_type

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