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Updated: Nov 19, 2025

Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Ese-3 contributes to colon cancer progression by downregulating EHD2 and transactivating INPP4B
Junqiang Li1, Jing Yang1, Lei Hua1
1Department of Oncology, Tangdu Hospital, Air Force Medical University Xi'an 710038, Shaanxi, China.
Abstract:
Epithelium-specific Ets protein 3 (Ese-3), a member of the Ets family of transcription factors, plays an important role in the development of cancers. However, little is known concerning its role in colon cancer (CC). In this study, we demonstrate that the expression of Ese-3 is upregulated in CC tissues and elevated Ese-3 expression is relationship with advanced T stage (P=0.037) and poor disease-free survival (DFS, P=0.044). Univariate and multivariate cox regression analyses show that Ese-3 expression may be an independent prognostic value for CC patients. Moreover, Ese-3 knockdown suppresses CC cell proliferation in vitro and in vivo, while Ese-3 overexpression has the opposite result. Further, we first demonstrate that EHD2 and INPP4B are the downstream genes of Ese-3. Subsequent investigation find that EHD2 is downregulated in CC tissues and knockdown of EHD2 significantly increase CC cell proliferation in vitro and vivo. Our findings reveal that Ese-3 promotes CC cell proliferation by downregulating EHD2 and transactivating INPP4B, and targeting the pathway may be a promising therapeutic target for CC patients.
Insights
Epithelium-specific Ets protein 3 (Ese-3) is upregulated in colon cancer (CC), promoting tumor growth by downregulating EHD2. Targeting this pathway offers a potential therapeutic strategy for CC patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Epithelium-specific Ets protein 3 (Ese-3) is an Ets family transcription factor implicated in various cancers.
- The specific role of Ese-3 in colon cancer (CC) pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the role and mechanism of Ese-3 in colon cancer development.
- To identify downstream targets of Ese-3 in CC.
Main Methods:
- Analysis of Ese-3 expression in CC tissues.
- In vitro and in vivo experiments involving Ese-3 knockdown and overexpression in CC cells.
- Investigation of downstream genes EHD2 and INPP4B.
Main Results:
- Ese-3 expression is upregulated in CC tissues and correlates with advanced T stage and poorer disease-free survival.
- Ese-3 knockdown inhibits CC cell proliferation, while overexpression enhances it.
- Ese-3 downregulates EHD2 and transactivates INPP4B, with EHD2 downregulation promoting CC cell proliferation.
Conclusions:
- Ese-3 promotes colon cancer cell proliferation by downregulating EHD2 and transactivating INPP4B.
- Ese-3 serves as an independent prognostic marker for CC patients.
- Targeting the Ese-3/EHD2/INPP4B pathway presents a potential therapeutic avenue for colon cancer.
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