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Ultrasound-Guided Orthotopic Implantation of Murine Pancreatic Ductal Adenocarcinoma
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E2F1-Driven WDHD1 Transcription Enhances Cell-Cycle Progression and Promotes Pancreatic Cancer Progression
Xiaojuan Yang1,2, Zhiwei Zhang1,3, Shuangjuan Lv2
1Department of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu 610041, China.
Current Oncology (Toronto, Ont.)
|April 27, 2026
Summary
WD repeat and HMG-box DNA-binding protein 1 (WDHD1) drives pancreatic cancer by promoting cell proliferation and cycle progression. Inhibiting WDHD1 suppresses tumor growth and induces apoptosis, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- WD repeat and HMG-box DNA-binding protein 1 (WDHD1) is an oncogene implicated in various cancers.
- The specific role and mechanisms of WDHD1 in pancreatic cancer progression were previously uninvestigated.
Purpose of the Study:
- To elucidate the function and molecular mechanisms of WDHD1 in pancreatic cancer.
- To determine the relationship between WDHD1, E2F1, and cell cycle regulators in pancreatic cancer.
Main Methods:
- Differential gene expression analysis using TCGA pancreatic cancer data.
- In vitro cellular assays (proliferation, flow cytometry, apoptosis) and in vivo xenograft models.
- Western blotting to assess protein levels of WDHD1, CDK4, cyclin D1, and E2F1.
Main Results:
- WDHD1 expression is significantly upregulated in pancreatic cancer tissues and cells.
- WDHD1 knockdown inhibits proliferation, induces apoptosis, and causes G1 cell-cycle arrest.
- WDHD1 promotes CDK4 and cyclin D1 expression; E2F1 upregulates WDHD1, driving cell cycle progression.
Conclusions:
- E2F1 promotes pancreatic cancer progression by upregulating WDHD1.
- WDHD1 enhances CDK4-cyclin D1 complex expression, driving proliferation and cell-cycle progression.
- Targeting WDHD1 may represent a novel therapeutic strategy for pancreatic cancer.
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