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 Carcinogjournal_title
Molecular carcinogenesisauthors
He L,Zhang J,Jiang L,Jin C,Zhao Y,Yang G,Jia Ldoi
10.1002/mc.20664subject
Has Abstractpub_date
2010-10-01 00:00:00pages
882-91issue
10eissn
0899-1987issn
1098-2744journal_volume
49pub_type
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更新日期:2013-06-01 00:00:00
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更新日期:1992-01-01 00:00:00
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pub_type: 杂志文章,随机对照试验
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更新日期:2016-03-01 00:00:00
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