PD-1 Antitumor Immunity against Murine H22 Hepatocarcinoma In vivo

PD-1 Antitumor Immunity against Murine H22 Hepatocarcinoma In vivo

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Author(s)

Author(s): Leilei Liang, Fuping Guan, Yinlin Ge

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DOI: 10.18483/ijSci.1591 168 470 71-76 Volume 7 - Mar 2018

Abstract

Objective: To explore the role of PD-1 expression level on the growth of hepatocarcinoma line H22. Methods: Tumor-bearing mice model was established with H22 cells in ICR mice. The model mice were randomly divided into two groups, control group and PD-1 interference group (PD-1-siRNA). The control group was injected transfection reagent, wherase the PD-1-siRNA was given the transfection reagent with PD-1-siRNA. Observed the life condition and tumor growth of mice, measured and recorded the tumor volume. The mRNA expression levels of PD-L1, PD-L2, P53, caspase-3 and IL-6 in tumor tissue were detected by real time fluorescence quantitative PCR (qPCR) technique. The expression of IFN-γ cytokines in spleen and tumor tissue was detected by ELISA. The ratio of Bax and Bcl-2 protein was detected by Western Blot to analyze the effect of PD-1-siRNA on tumor cell apoptosis. Results: Compared with control group, mice of PD-1-siRNA in better quality of life, survival time prolonged and the tumor volume of mouse was significantly reduced. The mRNA expression levels of PD-L1, PD-L2, P53 and caspase-3 were increased, others, IL-6 expression level was significantly decreased. The expression level of IFN-γ was up-regulated in spleen and tumor tissues. Western blot shown that the ratio of Bax and Bcl-2 was significantly increased. Conclusion: Interfere of PD-1 expression can effectively inhibit the growth of hepatocarcinoma cell H22 in mice.

Keywords

PD-1-siPD-1, PD-L1, Immunotherapy, H22 hepatoma cells, IFN-γ

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International Journal of Sciences is Open Access Journal.
This article is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) License.
Author(s) retain the copyrights of this article, though, publication rights are with Alkhaer Publications.

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