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Kang FB, Wang L, Jia HC, et al. B7-H3 promotes aggression and invasion of hepatocellular carcinoma by targeting epithelial-to-mesenchymal transition via JAK2/STAT3/Slug signaling pathway. Cancer Cell Int. 2015;15:45doi: 10.1186/s12935-015-0195-z.
Kang, F. B., Wang, L., Jia, H. C., Li, D., Li, H. J., Zhang, Y. G., & Sun, D. X. (2015). B7-H3 promotes aggression and invasion of hepatocellular carcinoma by targeting epithelial-to-mesenchymal transition via JAK2/STAT3/Slug signaling pathway. Cancer cell international, 1545. https://doi.org/10.1186/s12935-015-0195-z
Kang, Fu-Biao, et al. "B7-H3 promotes aggression and invasion of hepatocellular carcinoma by targeting epithelial-to-mesenchymal transition via JAK2/STAT3/Slug signaling pathway." Cancer cell international vol. 15 (2015): 45. doi: https://doi.org/10.1186/s12935-015-0195-z
Kang FB, Wang L, Jia HC, Li D, Li HJ, Zhang YG, Sun DX. B7-H3 promotes aggression and invasion of hepatocellular carcinoma by targeting epithelial-to-mesenchymal transition via JAK2/STAT3/Slug signaling pathway. Cancer Cell Int. 2015 Apr 21;15:45. doi: 10.1186/s12935-015-0195-z. eCollection 2015. PMID: 25908926; PMCID: PMC4407415.
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Cancer Cell Int. 2015 Apr 21;15:45. doi: 10.1186/s12935-015-0195-z. eCollection 2015.

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

Cancer cell international

Fu-Biao Kang, Ling Wang, Heng-Chuan Jia, Dong Li, Hai-Jun Li, Yin-Ge Zhang, Dian-Xing Sun

Affiliations

  1. Department of Liver Diseases, Bethune International Peace Hospital, Shijiazhuang, Hebei People's Republic of China.
  2. Chinese PLA Medical School, Chinese PLA General Hospital, Beijing, People's Republic of China.
  3. Cancer Research Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei People's Republic of China.

PMID: 25908926 PMCID: PMC4407415 DOI: 10.1186/s12935-015-0195-z

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

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