Research Paper Volume 15, Issue 20 pp 11489—11507
Anti-cancer targets and molecular mechanisms of formononetin in treating osteosarcoma based on network pharmacology
- 1 Department of Science and Education, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong, China
- 2 Guangdong Engineering Research Center for Translation of Medical 3D Printing Application, Guangdong Provincial Key Laboratory of Medical Biomechanics, National Key Discipline of Human Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China
- 3 The Affiliated Guangdong Second Provincial General Hospital of Jinan University, Guangzhou, China
- 4 Department of Hematology, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong, China
- 5 Department of Ultrasound, Institute of Ultrasound in Musculoskeletal Sports Medicine, Guangdong Second Provincial, General Hospital, Guangzhou, Guangdong, China
- 6 Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China
Received: May 30, 2023 Accepted: October 2, 2023 Published: October 20, 2023
https://doi.org/10.18632/aging.205139How to Cite
Copyright: © 2023 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Osteosarcoma (OS) is a multifactorial bone malignancy that accounts for most cancers in children and adolescents. Formononetin has been proven to exhibit various pharmacological effects including anti-tumor, anti-obesity, anti-inflammation, and neuroprotective effects. Few studies have examined the pharmacological activities of formononetin in OS treatment, but the mechanism has not yet been completely elucidated. Network pharmacology is a new method based on the theory of system biology for analyzing the network of biological systems and selecting specific signal nodes for multi-target drug molecular design. Here, we used network pharmacology to explore the possible mechanism of formononetin in OS treatment. Human OS cell line MG63 was processed with four concentrations (0, 2, 5, 8 μg/mL) of formononetin. Subsequently, an MTT assay was performed to test cell proliferation and a scratch test was used to evaluate the migration ability of cancer cells. Caspase-3, p53, p21, and bcl-2 expression levels incubated with different concentrations of formononetin in MG63 cells were determined using Western blotting. After treated with formononetin for 48 h, MG63 cells exhibited marked apoptosis. The results revealed that certain concentrations of formononetin significantly exerted inhibitory effects on MG63 cell proliferation. Furthermore, formononetin decreased the bcl-2 level in MG63 cells but increased caspase-3, p21, and p53 levels in a concentration-dependent manner. Additionally, formononetin suppressed the expression of SATB2. Therefore, formononetin could dose-dependently inhibit MG63 cell proliferation and induce apparent cell apoptosis, providing a candidate treatment for OS, whereas SATB2 could be a potential prognostic biomarker for screening OS and therapeutic target of formononetin.