NF-κB pathways are involved in M1 polarization of RAW 264.7 macrophage by polyporus polysaccharide in the tumor microenvironment.
NF-κB pathways are involved in M1 polarization of RAW 264.7 macrophage by polyporus polysaccharide in the tumor microenvironment.
复制标题
NF-kappa B 通路参与肿瘤微环境中猪苓多糖对 RAW 264.7 巨噬细胞的 M1 极化
DOI:
10.1371/journal.pone.0188317
复制
发表时间:
2017
期刊:
影响因子:
3.7
通讯作者:
Zeng X
中科院分区:
文献类型:
--
作者:
Liu CP;Zhang X;Tan QL;Xu WX;Zhou CY;Luo M;Li X;Huang RY;Zeng X
Bladder cancer is one of the most malignant tumors closely associated with macrophages. Polyporus polysaccharide (PPS) has shown excellent efficacy in treating bladder cancer with minimal side effects. However, the molecular mechanisms underlying the effects of PPS in inhibiting bladder cancer remain unclear. In this study, we used macrophages cultured alone or with T24 human bladder cancer cell culture supernatant as study models. We found that PPS enhanced the activities of IFN-γ-stimulated RAW 264.7 macrophages, as shown by the release of inducible nitric oxide synthase (INOS), secretion of tumor necrosis factor (TNF)-α and interleukin (IL)-6, phagocytosis activity, as well as expression of M1 phenotype indicators, such as CD40, CD284 and CD86. PPS acted upstream in activation cascade of nuclear factor (NF)-κB signaling pathways by interfering with IκB phosphorylation. In addition, PPS regulated NF-κB (P65) signaling by interfering with Toll-like receptor (TLR)-4, INOS and cyclooxygenase (COX)-2. Our results indicate that PPS activates macrophages through TLR4/NF-κB signaling pathways.
登录
查看更多内容
DOI:
10.1007/s00262-016-1810-0
发表时间:
2016-07
期刊:
Cancer immunology, immunotherapy : CII
影响因子:
--
作者:
Kalathil SG;Thanavala Y
通讯作者:
Thanavala Y
影响因子:
4.3
作者:
Julia Pedraza-Brindis, Eliza;Sanchez-Reyes, Karina;Cesar Ortiz-Lazareno, Pablo
通讯作者:
Cesar Ortiz-Lazareno, Pablo
影响因子:
3.4
作者:
Price, Lisa A.;Wenner, Cynthia A.;Novack, Jeffrey P.
通讯作者:
Novack, Jeffrey P.
影响因子:
11.2
作者:
Mao, Yumeng;Poschke, Isabel;Kiessling, Rolf
通讯作者:
Kiessling, Rolf
影响因子:
1.2
作者:
Kołodziej A;Krajewski W;Matuszewski M;Tupikowski K
通讯作者:
Tupikowski K