Interferon Gamma Inhibits CXCL8-Induced Proliferation and Migration of Pancreatic Cancer BxPC-3 Cell Line via a RhoGDI2/Rac1/NF-kB Signaling Pathway
Interferon Gamma Inhibits CXCL8-Induced Proliferation and Migration of Pancreatic Cancer BxPC-3 Cell Line via a RhoGDI2/Rac1/NF-kB Signaling Pathway
复制标题
干扰素 Gamma 通过 RhoGDI2/Rac1/NF-kB 信号通路抑制 CXCL8 诱导的胰腺癌 BxPC-3 细胞系的增殖和迁移
DOI：
10.1089/jir.2018.0070
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Cao LiPing
中科院分区：
文献类型：
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作者：
Zhang Mingjie;Ding Guoping;Zhou Liangjing;Shen Tao;Xu Xiaodong;Zhao Ting;Jia Shengnan;Cao LiPing
Interferon gamma (IFN-γ) is a dimeric soluble cytokine and the only type II interferon. Accumulated evidence suggests that IFN-γ inhibits tumor progression. This study investigated the effects of IFN-γ on the proliferation and migration of pancreatic cancer (PC) cells and the underlying mechanism. IFN-γ treatment decreased the expression and secretion of CXCL8 in BxPC-3 PC cells, suppressed the proliferation and migration of these cells, and enhanced their apoptosis, as determined by increased levels of cleaved Caspase-8 and Bax together with reduced expression of Bcl-2. These effects were abolished by overexpression of CXCL8. Moreover, IFN-γ treatment downregulated RhoGDI2 expression. Depletion of RhoGDI2 and Rac1 by using small interfering RNAs and inhibition of NF-κB by BMS-345541 (an IκB kinase [IKK] inhibitor) suppressed expression of CXCL8. Our results indicate that IFN-γ inhibits the proliferation and migration of PC cells by suppressing CXCL8 expression via a RhoGDI2/Rac1/NF-κB signaling pathway.
