Research Paper Volume 16, Issue 16 pp 12008—12028
Elucidation of the anti-colorectal cancer mechanism of Atractylodes lancea by network pharmacology and experimental verification
- 1 Affiliated Qingyuan Hospital (Qingyuan People’s Hospital), Guangzhou Medical University, Qingyuan 511518, Guangdong, China
- 2 Department of Histology and Embryology, Faculty of Basic Medical Sciences, Guilin Medical University, Guilin 541000, Guangxi, China
- 3 Faculty of Public Health, Guilin Medical University, Guilin 541000, Guangxi, China
- 4 Faculty of Basic Medical Sciences, Dali University, Dali 671003, Yunnan, China
- 5 Department of Pharmacy, Guilin Medical University, Guilin 541000, Guangxi, China
Received: December 4, 2023 Accepted: July 13, 2024 Published: August 22, 2024
https://doi.org/10.18632/aging.206075How to Cite
Copyright: © 2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Atractylodes lancea which was listed in “Shennong’s Materia Medica” and could be used to treat gastrointestinal-associated diseases. However, its roles, core and active ingredients, and mechanisms in treatment of colorectal cancer (CRC) were still unknown. Therefore, network pharmacology and experimental validation were used to clarify the effects, core active ingredients and molecular mechanisms of Atractylodes lancea. We found that Atractylodes lancea has 28 effective active components and 213 potential targets. Seventy-three genes which demonstrate interaction between the Atractylodes lancea and CRC were confirmed. Enrichment analysis showed that 2033 GO biological process items and 144 KEGG pathways. Survival and molecular docking analysis revealed that luteolin as the core component interacted with these genes (Matrix metalloproteinase 3 (MMP3), Matrix metalloproteinase 9 (MMP9), Tissue inhibitor of metalloproteinases 1 (TIMP1), Vascular endothelial growth factor A (VEGFA)) with the lowest binding energy, and these genes were involved in building a prognostic model for CRC. Cellular phenotyping experiments showed that luteolin could inhibit the proliferation and migration of CRC cells and downregulate the expression of MMP3, MMP9, TIMP1, VEGFA probably by Phosphoinositide 3-kinase/ serine/threonine kinase Akt (PI3K/AKT) pathway. To conclude, Atractylodes lancea could inhibit proliferation and migration of CRC cells through its core active ingredient (luteolin) to suppress the expression of MMP3, MMP9, TIMP1, VEGFA probably by PI3K/AKT pathway.