4.7 Article

Expression of B7-H6 expression in human hepatocellular carcinoma and its clinical significance

Journal

CANCER CELL INTERNATIONAL
Volume 18, Issue -, Pages -

Publisher

BMC
DOI: 10.1186/s12935-018-0627-7

Keywords

B7-H6; HCC; Immunohistochemistry; RNAI; Cancer progression

Categories

Funding

  1. National Natural Science Foundation of China [81301960, 31701111]
  2. Key R&D Project of Science and Technology Department of Jiangsu Province [BE2015633]
  3. Changzhou High-Level Medical Talents Training Project [2016CZBJ001]
  4. Jiangsu Key Laboratory of Medical Science and Laboratory Medicine [JSKLM-2014-003]
  5. Changzhou Science and Technology Project (Applied Based Research) [CJ20160021]

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Background: Recent studies have suggested that B7-H6, a new member of the B7 family of ligands, not only is a crucial regulator of NK cell-mediated immune responses but also has important clinical implications due to its abnormal expression in many human cancers. We have previously reported that higher B7-H6 expression levels in ovarian cancer tissues are positively correlated with tumor metastasis and cancer progression. To date, the expression of B7-H6 in human hepatocellular carcinoma (HCC) and the clinical significance of B7-H6 expression still remain elusive. Methods: In the present study, the expression level of B7-H6 was examined in both HCC tissues and HCC cell lines (HepG2 and SMMC-7721). And the clinical significance of B7-H6 was analyzed as well. Results: Our results revealed that B7-H6 was expressed abnormally in HCC tissues, which was greatly related to tumor size. The TCGA data also showed that the B7-H6 mRNA expression level was significantly negatively correlated with the survival of HCC patients. Next, to investigate the functions of B7-H6 in HCC, we successfully constructed B7-H6 knockdown expression human HCC cell lines using the RNA interference technology. Our studies showed that reduced expression of B7-H6 in HepG2 and SMMC-7721 cells significantly attenuated cell proliferation as well as cell migration and invasion. Besides, depletion of B7-H6 greatly induced cell cycle arrest at G1 phase. And also B7-H6 knockdown in HCC cell lines dramatically decreased the C-myc, C-fos and Cyclin-D1 expression. Conclusions: Our present findings suggested that B7-H6 played an important role in oncogenesis of HCC on cellular level, and B7-H6 could be employed to develop immunotherapeutic approaches targeting this malignancy.

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