ArticleOncology letters2020
DEPDC1B promotes migration and invasion in pancreatic ductal adenocarcinoma by activating the Akt/GSK3β/Snail pathway.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- Can Complex 3D Models Effectively Replace 2D and Animal Models to Investigate the Microbe-Tumor-Immune Axis in Pancreatic Cancer Studies?Nutrients · 2026Review
- Targeting MTPN sensitizes pancreatic cancer of wild-type BRCA1/2 to Cisplatin-based chemotherapy.Cancer gene therapy · 2025Article
- Isoleucyl-tRNA synthetase 2 promotes pancreatic ductal adenocarcinoma proliferation and metastasis by stabilizing β-catenin.Genes & diseases · 2025Article
- DEPDC1B: A novel tumor suppressor gene associated with immune infiltration in colon adenocarcinoma.Cancer medicine · 2024Article
- Active compounds of Caodoukou () inhibit the migration, invasion and metastasis of human pancreatic cancer cells by targeting phosphoinosmde-3-kinase/ protein kinase B/mammalian target of rapamycin pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- DEPDC1B is involved in the proliferation, metastasis, cell cycle arrest and apoptosis of colon cancer cells by regulating NUP37.Molecular medicine reports · 2023Article
- Article
- DEPDC1B promotes colorectal cancer via facilitating cell proliferation and migration while inhibiting apoptosis.Cell cycle (Georgetown, Tex.) · 2023Article
- Vitamin C Suppresses Pancreatic Carcinogenesis through the Inhibition of Both Glucose Metabolism and Wnt Signaling.International journal of molecular sciences · 2022Article
- DEPDC1B Promotes Melanoma Angiogenesis and Metastasis through Sequestration of Ubiquitin Ligase CDC16 to Stabilize Secreted SCUBE3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- MYC Inhibition Halts Metastatic Breast Cancer Progression by Blocking Growth, Invasion, and Seeding.Cancer research communications · 2022Article
- DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes.Frontiers in oncology · 2022Article
- High Expression of DEPDC1B Predicts Poor Prognosis in Lung Adenocarcinoma.Journal of inflammation research · 2022Article
- Up-Regulated MISP Is Associated With Poor Prognosis and Immune Infiltration in Pancreatic Ductal Adenocarcinoma.Frontiers in oncology · 2022Article
- Identification and Validation of DEPDC1B as an Independent Early Diagnostic and Prognostic Biomarker in Liver Hepatocellular Carcinoma.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal disease, which frequently presents with distant metastasis. Further understanding of the molecular mechanism of PDAC is helpful to uncover novel and effective therapeutic strategies. DEP domain containing 1B (DEPDC1B) is known to play a role in the carcinogenesis and metastasis of several common types of cancer; however, its biological function and molecular mechanism in PDAC progression remain unclear. In the present study, the expression levels of DEPDC1B were detected in 79 pairs of PDAC and adjacent non-cancerous tissues. Patients with PDAC that exhibited higher DEPDC1B expression levels, were shown to have a poorer prognosis. Functional studies showed that knocking down DEPDC1B inhibited PDAC cell migration and invasion, while overexpressing DEPDC1B promoted these processes. Western blotting analysis and immunofluorescence demonstrated that DEPDC1B overexpression induced the epithelial-to-mesenchymal transition (EMT). Further mechanistic studies revealed that DEPDC1B was able to activate the Akt/glycogen synthase kinase-3β (GSK3β)/Snail signaling pathway. In conclusion, the results of the present study showed that DEPDC1B may serve as an oncogene that contributes to PDAC cell migration and invasion by inducing EMT via Akt/GSK3β/Snail pathway activation.
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