Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10900092 | Cancer Letters | 2011 | 10 Pages |
Abstract
Macrophages play an important role in tumor inflammatory microenvironment, lipoxin (LX), the 'stop signal' for inflammation, has been extensively studied preclinically for its anti-inflammatory or inflammatory pro-resolving effect. Here, we showed that LXA4 could promote the apoptosis and inhibit the proliferation, migration and angiogenesis of HepG2 hepatocarcinoma cells stimulated by lipopolysaccharide (LPS) or activated macrophage-conditioned media (ACM). Moreover, BML-111, the analog of LXA4, effectively inhibited the proliferation, invasion and angiogenesis of tumor in H22 hepatocarcinoma cell bearing mice. These results showed that LXA4 could be a possible candidate for liver cancer therapy, and blocking the activation of macrophages would be an effective drug target.
Keywords
NF-κBLOXsLXSHuman acute monocytic leukemia cell lineH22nucleosteminLXA4U937RAW264.7FPRL1THP-1ECLACMTBSHepG2NSAIDSPBSLPSFBSC23BSACCmDMSOPMAbovine serum albuminenhanced chemiluminescenceTAMTris-buffered salineELISAEnzyme-linked immunosorbent assayHuman hepatocarcinoma cell lineNon-steroidal anti-inflammatory drugsDimethyl sulfoxidefetal bovine serumVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)phorbol myristate acetatelipopolysaccharideLipoxinslipoxygenaseslipoxinlipoxin A4Tumor-associated macrophagePhosphate-buffered salineHepatocarcinoma
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Authors
Hua Hao, Miao Liu, Ping Wu, Lei Cai, Ke Tang, Pan Yi, Yongsheng Li, Ying Chen, Duyun Ye,