Annexin II promotes invasion and migration of human hepatocellular carcinoma cells in vitro via its interaction with HAb18G/CD147

HAb18G/CD147, a member of the immunoglobulin family enriched on the surface of tumor cells, is reported to be correlated with invasion, metastasis, growth, and survival of malignant cells. Here, we found that annexin II, a 36‐kDa Ca2+‐ and phospholipid‐binding protein and in vivo substrate for tyros...

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Published inCancer science Vol. 101; no. 2; pp. 387 - 395
Main Authors Zhao, Pu, Zhang, Wei, Tang, Juan, Ma, Xiao‐Kui, Dai, Jing‐Yao, Li, Yong, Jiang, Jian‐Li, Zhang, Si‐He, Chen, Zhi‐Nan
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.02.2010
Blackwell
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ISSN1347-9032
1349-7006
1349-7006
DOI10.1111/j.1349-7006.2009.01420.x

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Summary:HAb18G/CD147, a member of the immunoglobulin family enriched on the surface of tumor cells, is reported to be correlated with invasion, metastasis, growth, and survival of malignant cells. Here, we found that annexin II, a 36‐kDa Ca2+‐ and phospholipid‐binding protein and in vivo substrate for tyrosine kinase and PKC, is a new interaction protein of HAb18G/CD147 in human hepatocellular carcinoma (HCC) cells. In the present study, we explored the unclear role of annxin II in HCC invasion and migration and the interaction effects between HAb18G/CD147 and annexin II. Our data show that downregulation of annexin II in HCC cells significantly decreased the secretion of MMP, migration ability, and invasive potential, and affected the cytoskeleton rearrangement of tumor cells. The MMP‐2 level and invasive potential of HCC cells were regulated by both annexin II and HAb18G/CD147. Also, interaction effects exist between the two molecules in tumor progression, including MMP‐2 production, migration, and invasion. These results suggest that annexin II promotes the invasion and migration of HCC cells in vitro, and annexin II and HAb18G/CD147 interact with each other in the same signal transduction pathway working as a functional complex in tumor progression. (Cancer Sci 2009)
Bibliography:These authors contributed equally to this work.
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ISSN:1347-9032
1349-7006
1349-7006
DOI:10.1111/j.1349-7006.2009.01420.x