التفاصيل البيبلوغرافية
| العنوان: |
Microcystin-LR-Induced Interaction between M2 Tumor-Associated Macrophage and Colorectal Cancer Cell Promotes Colorectal Cancer Cell Migration through Regulating the Expression of TGF-β1 and CST3. |
| المؤلفون: |
Jiang, Xinying1 (AUTHOR), Zhang, Hailing1 (AUTHOR), Zhang, Hengshuo1 (AUTHOR), Wang, Fan1 (AUTHOR), Wang, Xiaochang1 (AUTHOR), Ding, Tong1 (AUTHOR), Zhang, Xuxiang2 (AUTHOR) zhangxx@nju.edu.cn, Wang, Ting1 (AUTHOR) zhangxx@nju.edu.cn |
| المصدر: |
International Journal of Molecular Sciences. Jul2023, Vol. 24 Issue 13, p10527. 16p. |
| مصطلحات موضوعية: |
*CANCER cell migration, *COLORECTAL cancer, *CANCER cells, *CELL migration, *MACROPHAGES, *ROOT-tubercles, *CELL culture |
| مستخلص: |
Microcystin-LR (MC-LR) is a toxic secondary metabolite produced by cyanobacteria that has been demonstrated to promote colorectal cancer (CRC). However, the mechanism by which MC-LR enhances CRC in the tumor microenvironment (TME) is poorly understood. To elucidate its role in TME, a co-culture system was established using CRC cells and M2 macrophages in a Transwell chamber. The study found that MC-LR promotes CRC cell migration by upregulating TGF-β1 expression and secretion in M2 macrophages and downregulating CST3 in CRC cells. Neutralizing TGF-β1 increased CST3 expression in CRC cells, while overexpressing CST3 in CRC cells suppressed TGF-β1 expression in M2 macrophages, both of which weakened MC-LR-induced cellular motility in the co-culture system. In vivo, the mice in the MC-LR/AOM/DSS group had more tumor nodules, deeper tumor invasion, and higher M2 macrophage infiltration compared to the AOM/DSS group, and the expression of TGF-β1 and CST3 in tumors was consistent with the cellular level. Overall, this study provides insights into the regulatory mechanism of MC-LR on TME, revealing that MC-LR upregulates the expression and secretion of TGF-β1 in M2 macrophages, which in turn inhibits the expression of CST3 in CRC cells to promote migration. [ABSTRACT FROM AUTHOR] |
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