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Updated: Aug 29, 2025

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Published on: January 7, 2019
FOXM1 is regulated by DEPDC1 to facilitate development and metastasis of oral squamous cell carcinoma
Jing Qiu1, Yongping Tang1, Lan Liu1
1Department of Stomatology, Qingdao Municipal Hospital, Qingdao, Shandong, China.
Abstract:
The Disheveled, EGL-10, Pleckstrin domain containing 1 (DEPDC1) is a new oncogene that has recently been described. The mechanisms and functions of its expression are yet to be determined in oral squamous cell carcinoma (OSCC). In the present study, the impact of DEPDC1 on the growth and development of OSCC was investigated using animal models, cell lines and human tissue samples. Elevated DEPDC1 expression within cancer cell lines and human OSCC has been identified. Mechanistic examination showed that restored DEPDC1 expression in vivo and in vitro stimulated OSCC tumour development. In addition, FOXM1 interacts with DEPDC1 as indicated by co-immunoprecipitation and immunofluorescence testing. Functionally, DEPDC1 facilitated Wnt/β-catenin signal transduction and β-catenin protein nuclear expression. In summary, the DEPDC1, interacting with FOXM1 via Wnt/β-catenin signaling, the closely regulated OSCC pathogenesis, suggesting that targeting the novel DEPDC1/FOXM1/β-catenin complex is an essential OSCC therapeutic approach.
Insights
Disheveled, EGL-10, Pleckstrin domain containing 1 (DEPDC1) promotes oral squamous cell carcinoma (OSCC) growth by interacting with FOXM1 and activating Wnt/β-catenin signaling. Targeting this DEPDC1/FOXM1/β-catenin complex offers a potential therapeutic strategy for OSCC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The role of the DEPDC1 oncogene in oral squamous cell carcinoma (OSCC) remains largely undetermined.
- Understanding DEPDC1's function is crucial for developing targeted therapies for OSCC.
Purpose of the Study:
- To investigate the impact of DEPDC1 expression on OSCC growth and development.
- To elucidate the molecular mechanisms underlying DEPDC1's function in OSCC pathogenesis.
Main Methods:
- Utilized animal models, cell lines, and human OSCC tissue samples.
- Performed co-immunoprecipitation and immunofluorescence assays to study protein interactions.
- Analyzed DEPDC1's effect on Wnt/β-catenin signaling pathway activation.
Main Results:
- DEPDC1 expression was found to be elevated in OSCC cell lines and human tissues.
- Restored DEPDC1 expression promoted OSCC tumor development both in vivo and in vitro.
- DEPDC1 was identified to interact with FOXM1 and facilitate Wnt/β-catenin signaling, leading to increased nuclear β-catenin.
Conclusions:
- DEPDC1, in conjunction with FOXM1, drives OSCC pathogenesis through the Wnt/β-catenin signaling pathway.
- The novel DEPDC1/FOXM1/β-catenin complex represents a promising therapeutic target for oral squamous cell carcinoma.
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