ArticleFrontiers in oncology2019
High Expression of DEPDC1 Promotes Malignant Phenotypes of Breast Cancer Cells and Predicts Poor Prognosis in Patients With Breast Cancer.
Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 42 citations in OpenAlex.
- TCF7L2/DEPDC1 axis contributes to tumor progression by promoting cell proliferation, aerobic glycolysis, and immunosuppression in pancreatic cancer.Clinical and experimental medicine · 2026Article
- Methylation-regulated miR-374a-5p and miR-374b-5p suppress glycolysis and malignant progression of head and neck squamous cell carcinoma by targeting DEPDC1.Frontiers in oncology · 2026Article
- p53 inactivation drives breast cancer metastasis to the brain through SCD1 upregulation and increased fatty acid metabolism.Nature genetics · 2026Article
- DEP domain containing 1: a potential oncogenic driver.Biological research · 2025Article
- BC-predict: mining of signal biomarkers and production of models for early-stage breast cancer subtyping and prognosis.Frontiers in bioinformatics · 2025Article
- DEPDC1 facilitated malignant phenotypes and disease progression of liposarcoma by modulating KIF20A.Frontiers in endocrinology · 2025Article
- Roles of DEPDC1 in various types of cancer (Review).Oncology letters · 2024Review
- DEPDC1 as a metabolic target regulates glycolysis in renal cell carcinoma through AKT/mTOR/HIF1α pathway.Cell death & disease · 2024Article
- Wnt/β-Catenin Signaling Pathway in Pediatric Tumors: Implications for Diagnosis and Treatment.Children (Basel, Switzerland) · 2024Review
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- DEPDC1 as a crucial factor in the progression of human osteosarcoma.Cancer medicine · 2023Article
- Glycolysis-Related Gene Analyses Indicate That DEPDC1 Promotes the Malignant Progression of Oral Squamous Cell Carcinoma via the WNT/β-Catenin Signaling Pathway.International journal of molecular sciences · 2023Article
- Pan-cancer analysis ofAnnals of translational medicine · 2022Article
- FOXO3a‑modulated DEPDC1 promotes malignant progression of nephroblastoma via the Wnt/β‑catenin signaling pathway.Molecular medicine reports · 2022Article
- DEPDC1B collaborates with GABRD to regulate ESCC progression.Cancer cell international · 2022Article
- Upregulation of circ_0008812 and circ_0001583 predicts poor prognosis and promotes breast cancer proliferation.Frontiers in molecular biosciences · 2022Article
- Integrated transcriptome and network analysis identifies EZH2/CCNB1/PPARG as prognostic factors in breast cancer.Frontiers in genetics · 2022Article
- miR-455-5p enhances 5-fluorouracil sensitivity in colorectal cancer cells by targeting PIK3R1 and DEPDC1.Open medicine (Warsaw, Poland) · 2022Article
- DEP domain containing 1B (DEPDC1B) exerts the tumor promoter in hepatocellular carcinoma through activating p53 signaling pathway via kinesin family member 23 (KIF23).Bioengineered · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DEP domain containing 1 (DEPDC1) is a novel tumor-associated gene, which is aberrantly expressed in multiple types of cancer and involves in tumorigenesis and cancer progression. Here, we examined the functional involvement and underlying mechanism of DEPDC1 in breast cancer. In this study, the immunohistochemistry results demonstrated that DEPDC1 was high-expressed in breast cancer tissues compared with the paired adjacent normal breast tissues, and its tendency at protein level was consistent with mRNA level from TCGA data. Moreover, DEPDC1 mRNA level revealed the strongest association with poor prognosis and development in breast cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.