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A few days ago, the academic journal International Journal of Biological Macromolecules published a report by the Seaweed Chemistry and Marine Drugs Research Group of the Key Laboratory of Experimental Marine Biology of the Chinese Academy of Sciences on fucoidan sulfate as an immunostimulant to induce directional polarization of macrophages and improve the tumor microenvironment.
Study
to enhance the sensitivity of colon cancer to capecitabine chemotherapy treatment.
Study
to enhance the sensitivity of colon cancer to capecitabine chemotherapy treatment.
The results of this study show the great potential of FPS1M in tumor immunotherapy and suggest that FPS1M combined with capecitabine may be an alternative combination strategy
for the treatment of colon cancer.
Chemotherapy resistance is one of the most critical challenges in the treatment of colorectal cancer (CRC), and the occurrence and progression of chemotherapy resistance is closely related to
the tumor immune microenvironment (TIME).
Macrophages are the most important immunosuppressive cells that infiltrate into the tumor microenvironment and are the key to the resistance of CRC chemotherapy, macrophages account for about 30% of the total tumor volume, and show tumicidal M1 phenotype and tumor-promoting M2 in the tumor microenvironment phenotype, in which M2 macrophages are the main cell type
infiltrated into tumors.
Therefore, reprogramming or directional differentiation of macrophages into M1 phenotypes is an effective strategy
for regulating tumor immunity and killing tumors.
Zhang Quanbin's research group has long been committed to the preparation
and activity of fucoidan sulfate.
After preliminary screening, the team found that a high molecular weight fucoidan sulfate FPS1M can significantly induce the transformation of macrophage M1 phenotype, which promotes apoptosis
of colon cancer cells in vivo and in vitro.
In terms of mechanism, it was found that FPS1M was a strong stimulant of TLR4, and FPS1M significantly upregulated PI3K, AKT.
The phosphorylation level of mTOR and increased the expression of PPARγ indicate that FPS1M is mediated by activation of TLR4 PI3K-AKT-mTOR-PPARγ signaling axis, promote macrophage glycolysis, and regulate macrophage differentiation to M1 phenotype
.
The results of the study established a mouse subcutaneous inoculation tumor model, and the results showed that FPS1M increased the infiltration of M1 macrophages in tumor tissues and improved the immunosuppressive tumor microenvironment, compared with capecitabine alone, FPS1M The combination with the chemotherapy drug capecitabine significantly promoted the expression of Caspase9,Cleaved-PARP1 in tumor tissues, indicating that FPS1M improved the sensitivity of colon cancer to chemotherapy capecitabine
。
The first author of the study is Deng Zhenzhen, a doctoral student in the Key Laboratory of Experimental Marine Biology, and the corresponding authors are researcher Wu Ning and researcher
Zhang Quanbin.
The research was supported
by the National Natural Science Foundation of China and the Shandong Science and Technology Innovation Major Project.
Paper Information: Zhenzhen Deng, Ning Wu*, Qishan Suo, Jing Wang, Yang Yue, Lihua Geng, Quanbin Zhang*, 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.
https://doi.
org/10.
1016/j.
ijbiomac.
2022.
09.
201
Fig.
1 FPS1M induces M1 phenotypic transformation of macrophages
Fig.
2 FPS1M enhances the chemosensitivity of the chemotherapy drug capecitabine
Fig.
3 Molecular mechanism of fucoidan sulfate regulating tumor macrophage differentiation
