B7-H4 overexpression is essential for early hepatocellular carcinoma progression and recurrence
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Fu-Biao Kang1, Ling Wang2, Dian-Xing Sun1, Hai-Jun Li1, Dong Li1, Yan Wang1 and Ji-Wen Kang1
1The Liver Disease Diagnosis and Treatment Center, Bethune International Peace Hospital, Shijiazhuang, Hebei, P.R. China
2Department of Orthopedic Oncology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, P.R. China
Fu-Biao Kang, email: firstname.lastname@example.org
Keywords: hepatocellular carcinoma, B7-H4, cancer progression, cancer recurrence
Received: April 23, 2017 Accepted: August 09, 2017 Published: September 08, 2017
B7-H4, another member of costimulatory molecule, has been shown to be overexpressed in multiple types of tumors, including hepatocellular carcinoma (HCC). However, the specific biological role of B7-H4 in HCC still needs to be further explored. In this study, we observed that B7-H4 was highly overexpressed in HCC tissues and cells, and its overexpression strongly correlated with patient's TNM stage, overall survival and early recurrence. Downregulation of B7-H4 significantly suppressed cell growth, invasion, and stemness of HCC by inducing apoptosis in the in vitro experiment. In addition, depletion of B7-H4 could help restore CD8+ T anti-tumor immunity by elevating the expression and secretion levels of CD107a, granzyme A, granzyme B, perforin and IFN-γ. In a xenografted mouse model of HCC, stable depletion of B7-H4 resulted in significantly smaller mean tumor volume and less mean tumor weight after 30 days of growth, compared to the control group. Together, our results provide insights into the diverse functions of B7-H4 involved in the pathogenesis, recurrence and anti-tumor immunity of HCC, indicating B7-H4 as a novel and effective approach for future treatment strategies that benefits anticancer therapy.
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