The final, formatted version of the article will be published soon.
ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Immunity and Immunotherapy
Volume 14 - 2024 |
doi: 10.3389/fonc.2024.1528454
This article is part of the Research Topic Big Data and Precision Medicine: Diagnosis and Treatment, Drug Discovery, and Integration of Multiple Omics View all 10 articles
DET induces apoptosis and suppresses tumor invasion in glioma cells via PI3K/AKT pathway
Provisionally accepted
Rui Zhao
1
Mengran Wang
1
Zeyu Wu
1
Panpan Zhao
1
Huiling Dong
1
Yue Su
1
Chenghui Zhao
1
Min Qi
1
Shizhang Ling
1,2*
Xiaochun Jiang
1,2*- 1 Translational Research Institute for Neurological Disorders, Department of Neurosurgery, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), Wuhu 241001, China, Wuhu, Anhui Province, China
- 2 The Institutes of Brain Science, Wannan Medical College, Higher Education Park, Wuhu 241002, Anhui, China, Wuhu, Anhui Province, China
Background: Gliomas, particularly glioblastomas (GBM), are highly aggressive with a poor prognosis and low survival rates. Currently, deoxyelephantopin (DET) has shown promising anti-inflammatory and anti-tumor effects. Using network clinical analysis, molecular docking, and pharmacology, this study aims to explore the primary targets and signaling pathways to identify novel GBM treatment approaches. Methods: Using PharmMapper, the chemical structure of DET was examined for possible targets after being acquired from PubChem. GBM-related targets were obtained through multi-omics approaches. A protein-protein interaction (PPI) network was constructed using Cytoscape and STRING, and target binding was evaluated through molecular docking. Enrichment analysis was conducted using Metascape. The effects of DET on GBM cell invasion, apoptosis, and proliferation were assessed through in vitro assays, including Transwell, EDU, CCK8, and flow cytometry. Western blot analysis was performed to examine the components of the PI3K/AKT signaling pathway. Results: Among the sixty-four shared targets identified, JUN and CCND1 were the most frequently observed. Enrichment analysis demonstrated that DET influenced the MAPK and PI3K/AKT signaling pathways. In Transwell assays, DET significantly inhibited the invasive behavior of glioma cells. Western blot analysis further confirmed the downregulation of EGFR, JUN, and PI3K/AKT. Conclusion: DET inhibits GBM cell invasion, proliferation, and apoptosis via modulating the PI3K/AKT signaling pathway, highlighting its potential as a novel therapeutic strategy for GBM treatment.
Keywords: Glioma, proliferation, Apoptosis, PI3K, invasion
Received: 14 Nov 2024; Accepted: 16 Dec 2024.
Copyright: © 2024 Zhao, Wang, Wu, Zhao, Dong, Su, Zhao, Qi, Ling and Jiang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Shizhang Ling, Translational Research Institute for Neurological Disorders, Department of Neurosurgery, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), Wuhu 241001, China, Wuhu, Anhui Province, China
Xiaochun Jiang, Translational Research Institute for Neurological Disorders, Department of Neurosurgery, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), Wuhu 241001, China, Wuhu, Anhui Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.