Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells
Oral squamous cell carcinoma (OSCC), an aggressive and poorly prognosed subtype of head and neck squamous cell carcinoma (HNSCC), has prompted urgent calls for innovative therapeutic approaches. Evodiamine (EVO), a natural alkaloid extracted from the Chinese herb <i>Evodia rutaecarpa</i>...
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2025-07-01
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| author | Gang Chen Hong-Liang Du Jia-Nan Liu Jie Cheng Jing Chen Xiao-Yang Yin Hu-Lai Wei Jing Wang |
| author_facet | Gang Chen Hong-Liang Du Jia-Nan Liu Jie Cheng Jing Chen Xiao-Yang Yin Hu-Lai Wei Jing Wang |
| author_sort | Gang Chen |
| collection | DOAJ |
| description | Oral squamous cell carcinoma (OSCC), an aggressive and poorly prognosed subtype of head and neck squamous cell carcinoma (HNSCC), has prompted urgent calls for innovative therapeutic approaches. Evodiamine (EVO), a natural alkaloid extracted from the Chinese herb <i>Evodia rutaecarpa</i>, has demonstrated significant potential in curbing tumor cell proliferation and slowing tumor expansion. However, its specific effects on cell senescence within the context of OSCC have remained shrouded in uncertainty. This study delves into the mechanisms of EVO’s impact on OSCC by harnessing databases such as the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), The Cancer Genome Atlas (TCGA), the Gene Expression Omnibus (GEO), and CellAge to pinpoint potential targets and carry out in-depth bioinformatics analysis. The findings reveal that EVO can markedly enhance the expression of the androgen receptor (AR) in OSCC cells, inducing cellular senescence and thereby inhibiting tumor progression. Furthermore, the research indicates that AR expression is considerably lower in OSCC tissues than in normal tissues. This low expression of AR in tumor tissues is closely associated with advanced clinical stages and unfavorable prognoses in HNSCC patients. These discoveries open up new avenues for therapeutic strategies, and suggest that AR holds promise as a potential therapeutic target for OSCC, and EVO may amplify its antitumor effects by enhancing AR-mediated cellular senescence in the treatment of OSCC. |
| format | Article |
| id | doaj-art-d6924f83c42b4394975c1102df9bce31 |
| institution | Matheson Library |
| issn | 1467-3037 1467-3045 |
| language | English |
| publishDate | 2025-07-01 |
| publisher | MDPI AG |
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| spelling | doaj-art-d6924f83c42b4394975c1102df9bce312025-07-25T13:18:47ZengMDPI AGCurrent Issues in Molecular Biology1467-30371467-30452025-07-0147755810.3390/cimb47070558Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC CellsGang Chen0Hong-Liang Du1Jia-Nan Liu2Jie Cheng3Jing Chen4Xiao-Yang Yin5Hu-Lai Wei6Jing Wang7School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, ChinaThe First Hospital of Lanzhou University, Lanzhou 730000, ChinaGeneral Practitioner Primary Training Base of the First Hospital of Lanzhou University, Lanzhou 730000, ChinaSchool of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, ChinaSchool of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, ChinaSchool of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, ChinaSchool of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, ChinaHospital of Stomatology, Lanzhou University, Lanzhou 730000, ChinaOral squamous cell carcinoma (OSCC), an aggressive and poorly prognosed subtype of head and neck squamous cell carcinoma (HNSCC), has prompted urgent calls for innovative therapeutic approaches. Evodiamine (EVO), a natural alkaloid extracted from the Chinese herb <i>Evodia rutaecarpa</i>, has demonstrated significant potential in curbing tumor cell proliferation and slowing tumor expansion. However, its specific effects on cell senescence within the context of OSCC have remained shrouded in uncertainty. This study delves into the mechanisms of EVO’s impact on OSCC by harnessing databases such as the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), The Cancer Genome Atlas (TCGA), the Gene Expression Omnibus (GEO), and CellAge to pinpoint potential targets and carry out in-depth bioinformatics analysis. The findings reveal that EVO can markedly enhance the expression of the androgen receptor (AR) in OSCC cells, inducing cellular senescence and thereby inhibiting tumor progression. Furthermore, the research indicates that AR expression is considerably lower in OSCC tissues than in normal tissues. This low expression of AR in tumor tissues is closely associated with advanced clinical stages and unfavorable prognoses in HNSCC patients. These discoveries open up new avenues for therapeutic strategies, and suggest that AR holds promise as a potential therapeutic target for OSCC, and EVO may amplify its antitumor effects by enhancing AR-mediated cellular senescence in the treatment of OSCC.https://www.mdpi.com/1467-3045/47/7/558evodiamineandrogen receptororal squamous cell carcinomasenescence |
| spellingShingle | Gang Chen Hong-Liang Du Jia-Nan Liu Jie Cheng Jing Chen Xiao-Yang Yin Hu-Lai Wei Jing Wang Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells Current Issues in Molecular Biology evodiamine androgen receptor oral squamous cell carcinoma senescence |
| title | Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells |
| title_full | Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells |
| title_fullStr | Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells |
| title_full_unstemmed | Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells |
| title_short | Evodiamine Boosts AR Expression to Trigger Senescence and Halt Proliferation in OSCC Cells |
| title_sort | evodiamine boosts ar expression to trigger senescence and halt proliferation in oscc cells |
| topic | evodiamine androgen receptor oral squamous cell carcinoma senescence |
| url | https://www.mdpi.com/1467-3045/47/7/558 |
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