褐藻糖胶
生物信息学
结直肠癌
癌症研究
生物
计算生物学
癌症
基因
生物化学
遗传学
多糖
作者
Jiaqi Liu,Yuexia Meng,Bihui Li,Pin Wang,Xiaowei Wan,Wenjun Huang,Rong Li
标识
DOI:10.1016/j.ijbiomac.2022.09.255
摘要
Ferroptosis, a type of iron-dependent cell death, has been linked with the occurrence and progression of malignant tumors, including colorectal cancer (CRC). Fucoidan, an algal fucose-rich molecule, has been discovered preclinically to have an anti-CRC signature. Although some underlying mechanisms are reported, many signaling pathways associated with ferroptosis in fucoidan treatment of CRC are still unidentified. In this study, we applied network pharmacology and molecular docking technologies to unmask and identify the medication targets and pharmaceutical mechanisms involved in ferroptosis in fucoidan-treated CRC. 19 ferroptosis-related core targets were identified and enrichment analysis indicated their contribution to pharmacological actions and mechanisms in fucoidan treatment of CRC, including ferroptosis-related signaling pathways. Additional molecular docking verification confirmed that fucoidan docked well with ranked core targets, including transcription factor p65 (RELA), interleukin-1 beta (IL1B), and interleukin-6 (IL6). These in silico findings were validated experimentally in CRC cells following fucoidan treatment. RELA, IL1B, and IL6 expressed positively in human CRC samples. In conclusion, the pharmacological mechanisms of fucoidan in treating CRC may be achieved through multiple biological targets and multiple molecular pathways associated with ferroptosis. Thus, these preclinical findings have laid a theoretical foundation for further research and clinical treatment of CRC using fucoidan.
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