Research Papers:

DlgR2 knockdown boosts dendritic cell activity and inhibits hepatocellular carcinoma tumor in-situ growth

Zhen Lu, Yun-Hong Xia _, Min Zhao, Bing Zhang, Wen-Ting Dai, Lu Ding, Li-Xia Hu, Jin-Ling Bi and Guo-Lin Jiang

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Oncotarget. 2017; 8:54993-55002. https://doi.org/10.18632/oncotarget.18990

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Zhen Lu1,*, Yun-Hong Xia2,*, Min Zhao3, Bing Zhang3, Wen-Ting Dai3, Lu Ding3, Li-Xia Hu3, Jin-Ling Bi3 and Guo-Lin Jiang4

1Department of General Surgery, The Fourth Affiliated Hospital, Anhui Medical University, Hefei, China

2Department of Oncology, The Fourth Affiliated Hospital, Anhui Medical University, Hefei, China

3Hefei Hospital, Anhui Medical University, Hefei, China

4Key Laboratory of Anhui Medical University, Hefei, China

*Co-first author

Correspondence to:

Yun-Hong Xia, email: [email protected], [email protected]

Keywords: hepatocellular carcinoma (HCC), dendritic cells, DIgR2, tumor immunity, oncotarget

Received: May 25, 2017     Accepted: June 16, 2017     Published: July 05, 2017


Tumor-specific hepatic stellate cells (tHSCs) positively participate in human hepatocellular carcinoma (HCC) tumorigenesis and progression. Our previous studies have shown that tHSCs co-culture with dendritic cells (DCs) induced DIgR2 (dendritic cell-derived immunoglobulin receptor 2) expression. The latter is a member of IgSF inhibitory receptor suppressing DCs-initiated antigen-specific T-cell responses. In the current study, we show that hepatic artery injection of DlgR2 siRNA significantly inhibited in-situ HCC xenograft growth in rat livers. Further, 5-FU-medied inhibition of in-situ HCC growth was dramatically sensitized with DlgR2 silence. DlgR2 siRNA injection indeed downregulated DlgR2 in ex-vivo cultured tumor-derived DCs (tDCs). More importantly, tDCs activity was boosted following DlgR2 siRNA. These cells presented with upregulated CD80, CD86 and MHC-II. Production of interleukin-12 and tumor necrosis factor-α was also increased in the DlgR2-silenced tDCs. We propose that DlgR2 knockdown likely boosts the activity of tumor-associated DCs, and inhibits growth of in-situ HCC xenografts.

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