Journal Article

Heme oxygenase-1: a molecular brake on hepatocellular carcinoma cell migration

C. Zou, H. Zhang, Q. Li, H. Xiao, L. Yu, S. Ke, L. Zhou, W. Liu, W. Wang, H. Huang, N. Ma, Q. Liu, X. Wang, W. Zhao, H. Zhou and X. Gao

in Carcinogenesis

Volume 32, issue 12, pages 1840-1848
Published in print December 2011 | ISSN: 0143-3334
Published online October 2011 | e-ISSN: 1460-2180 | DOI:
Heme oxygenase-1: a molecular brake on hepatocellular carcinoma cell migration

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Hepatocellular carcinoma (HCC) is a fatal disease with great public health impact worldwide. Heme oxygenase (HO)-1 has recently been reported as an important player in tumor angiogenesis and metastasis. However, the role of HO-1 in liver cancer metastasis is unclear. In this study, we explored genetic differences and downstream signal transduction pathways of HO-1 in liver cancer cell lines. HO-1 wild-type and mutant cell lines were generated from human liver cancer cell line HepG2. The overexpression of wild-type HO-1 decreased the migration of HepG2 cells. In contrast, the overexpression of mutant HO-1G143H increased the migration of the cancer cells. Interleukin (IL)-6 is one of the major downstream molecules that mediated this process because IL-6 expression and migration are suppressed by HO-1 and increased when HO-1 is knocked down by shRNA. In addition, we demonstrated carbon monoxide (CO) and p38MAPK are the cofactors in this signal pathway. In vivo animal model demonstrated HO-1 inhibited the tumor growth. In conclusion, in vitro and in vivo data show HO-1 inhibits the human HCC cells migration and tumor growth by suppressing the expression of IL-6. The heme degradation product CO is a cofactor in this process and inhibits p38MAPK phosphorylation.

Journal Article.  5907 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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