Fucoidan, as an immunostimulator promotes M1 macrophage differentiation and enhances the chemotherapeutic sensitivity of capecitabine in colon cancer
文献类型:期刊论文
作者 | Deng, Zhenzhen1,2,3,4; Wu, Ning1,2,5; Suo, Qishan2,4; Wang, Jing1,2,3; Yue, Yang1,2,3; Geng, Lihua1,2,3; Zhang, Quanbin1,2,3 |
刊名 | INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES |
出版日期 | 2022-12-01 |
卷号 | 222页码:562-572 |
ISSN号 | 0141-8130 |
关键词 | Capecitabine Tumor microenvironment Macrophages TLR4 Fucoidan |
DOI | 10.1016/j.ijbiomac.2022.09.201 |
通讯作者 | Wu, Ning(wuning@qdio.ac.cn) ; Zhang, Quanbin(qbzhang@qdio.ac.cn) |
英文摘要 | Chemotherapy resistance is one of the most critical challenges in colorectal cancer (CRC) treatment. The occurrence and development of chemotherapy resistance closely related to the tumor immune microenvironment (TIME). As the most important immunosuppressive immune cells infiltrating into the TIME, macrophages are essential for chemotherapy resistance in CRC treatment. In this study, we found that a kind of fucoidan (FPS1M) induced macrophages differentiation to the M1 phenotype, and this transformation promoted cancer cells apoptosis both in vitro and in vivo. TNF alpha is a key mediator of FPS1M-induced tumorcidal activity of macrophages. Mechanistically, as a stimulator of TLR4, FPS1M enhanced macrophages glycolysis and regulated macrophages differentiation to the M1 phenotype by the activation of TLR4 mediated PI3K/AKT/mTOR signaling axis. In addition, FPS1M improved the immunosuppressed tumor microenvironment by increasing the infiltration of M1 macrophages in tumor tissue, which was conducive to improving the sensitivity of tumor to chemotherapy. Collectively, our findings demonstrated that FPS1M has the great potential to be used in tumor immunotherapy. The results also suggested that the combination of FPS1M with capecitabine is an alternative therapy method for colon cancer. |
资助项目 | National Natural Science Foundation of China ; Major Scientific & Engineering Projects of Innovation in Shandong Province ; [81872906] ; [42176137] ; [2019JZZY010818] |
WOS研究方向 | Biochemistry & Molecular Biology ; Chemistry ; Polymer Science |
语种 | 英语 |
出版者 | ELSEVIER |
WOS记录号 | WOS:000876352600006 |
源URL | [http://ir.qdio.ac.cn/handle/337002/180539] |
专题 | 海洋研究所_实验海洋生物学重点实验室 |
通讯作者 | Wu, Ning; Zhang, Quanbin |
作者单位 | 1.Chinese Acad Sci, CAS, Qingdao 266071, Peoples R China 2.Chinese Acad Sci, Inst Oceanol, Ctr Ocean Mega Sci, Shandong Prov Key Lab Expt Marine Biol, Qingdao 266071, Peoples R China 3.Qingdao Natl Lab Marine Sci & Tech, Lab Marine Biol & Biotechnol, Qingdao 266071, Peoples R China 4.Univ Chinese Acad Sci, Beijing 100049, Peoples R China 5.Pilot Natl Lab Marine Sci & Technol, Lab Marine drugs & Biol Prod, Qingdao, Peoples R China |
推荐引用方式 GB/T 7714 | Deng, Zhenzhen,Wu, Ning,Suo, Qishan,et al. Fucoidan, as an immunostimulator promotes M1 macrophage differentiation and enhances the chemotherapeutic sensitivity of capecitabine in colon cancer[J]. INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES,2022,222:562-572. |
APA | Deng, Zhenzhen.,Wu, Ning.,Suo, Qishan.,Wang, Jing.,Yue, Yang.,...&Zhang, Quanbin.(2022).Fucoidan, as an immunostimulator promotes M1 macrophage differentiation and enhances the chemotherapeutic sensitivity of capecitabine in colon cancer.INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES,222,562-572. |
MLA | Deng, Zhenzhen,et al."Fucoidan, as an immunostimulator promotes M1 macrophage differentiation and enhances the chemotherapeutic sensitivity of capecitabine in colon cancer".INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES 222(2022):562-572. |
入库方式: OAI收割
来源:海洋研究所
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