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Cancer Cell International | Full text | B7-H3 promotes aggression and invasion of hepatocellular carcinoma by targeting epithelial-to-mesenchymal transition via JAK2/STAT3/Slug signaling pathway

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Primary research

B7-H3 promotes aggression and invasion of hepatocellular carcinoma by targeting epithelial-to-mesenchymal transition via JAK2/STAT3/Slug signaling pathway

Fu-biao Kang¹²^†, Ling Wang³^†, Heng-chuan Jia¹^†, Dong Li¹, Hai-jun Li¹, Yin-ge Zhang¹and Dian-xing Sun¹²^*

*Corresponding author: Dian-xing Sun sundianxing@hotmail.com
† Equal contributors

Author Affiliations

¹Department of Liver Diseases, Bethune International Peace Hospital, Shijiazhuang, Hebei, People’s Republic of China

²Chinese PLA Medical School, Chinese PLA General Hospital, Beijing, People’s Republic of China

³Cancer Research Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China

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Cancer Cell International 2015, 15:45 doi:10.1186/s12935-015-0195-z

Fu-biao Kang, Ling Wang and Heng-chuan Jia contributed equally to this work.

The electronic version of this article is the complete one and can be found online at:http://www.cancerci.com/content/15/1/45

Received:	30 April 2014
Accepted:	6 April 2015
Published:	21 April 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Abstract

Background

B7-homologue 3 (B7-H3), a recently identified immunoregulatory protein, has been shown to be overexpressed in human hepatocellular carcinoma (HCC). However, whether the dynamic expression pattern of B7-H3 contributes to early invasion of HCC is largely unknown. In addition, the biological roles of B7-H3 in HCC are still unclear. Herein, we are going to examine B7-H3 expression profile and its clinicopathological significance in primary and metastatic HCC, and further determine whether B7-H3 knockdown simulates different pathological states of HCC progression and metastasis.

Methods

Using immunohistochemistry, B7-H3 expression was studied on 116 HCC containing primary and metastatic HCCs. Survival curves and log-rank tests were used to test the association of B7-H3 expression with survival. HCC cells with B7-H3 depletion were established by RNA interference to investigate the effect of B7-H3 on cell proliferation, apoptosis, migration and invasion in vitro.

Results

Statistical analysis of clinical cases revealed that B7-H3 high expression group had inclinations towards late TNM stage, the presence of vascular invasion, lymph metastasis, and the formation of microsatellite tumors. Increased intensity of tumor B7-H3 staining was detected more significantly in metastatic HCC tumors. Consistently in experiments performed in vitro, B7-H3 was able to stimulate the wound healing, metastasis and invasion of hepatoma cells by targeting epithelial-to-mesenchymal transition (EMT) via JAK2/Stat3/Slug signaling pathway, while no obvious influence on cell growth and apoptosis.

Conclusion

B7-H3 in the regulation of the metastatic capacity of HCC cells makes itself a promising therapeutic target for anti-metastasis therapy.

Keywords:

Hepatocellular carcinoma; B7-H3; Invasion; Epithelial-To-Mesenchymal Transition; JAK/STAT signaling pathway

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