ArticleAging2020
The cross-talk between DDR1 and STAT3 promotes the development of hepatocellular carcinoma.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed.
- Article
- E3 ubiquitin ligase NEDD4L inhibits epithelial-mesenchymal transition by suppressing the β-catenin/HIF-1α positive feedback loop in chronic rhinosinusitis with nasal polyps.Acta pharmacologica Sinica · 2024Article
- Clinical significance of immunohistochemical expression of DDR1 and β-catenin in colorectal carcinoma.World journal of surgical oncology · 2023Article
- Deciphering STAT3 signaling potential in hepatocellular carcinoma: tumorigenesis, treatment resistance, and pharmacological significance.Cellular & molecular biology letters · 2023Review
- Focusing on discoidin domain receptors in premalignant and malignant liver diseases.Frontiers in oncology · 2023Review
- Glutamine metabolic reprogramming in hepatocellular carcinoma.Frontiers in molecular biosciences · 2023Review
- Collagen XV mediated the epithelial-mesenchymal transition to inhibit hepatocellular carcinoma metastasis.Journal of gastrointestinal oncology · 2022Article
- DDR1 promotes LoVo cell proliferation by regulating energy metabolism.Acta biochimica et biophysica Sinica · 2022Article
- Discoidin domain receptor 1a (DDR1a) confers 5-fluorouracil cytotoxicity in LoVo cell via PI3K/AKT/Bcl-2 pathway.Bioengineered · 2022Article
- Discoidin domain receptor 1 is a potential target correlated with tumor invasion and immune infiltration in gastric cancer.Frontiers in immunology · 2022Article
- Discoidin Domain Receptor 1, a Potential Biomarker and Therapeutic Target in Hepatocellular Carcinoma.International journal of general medicine · 2022Review
- The Collagen Receptor Discoidin Domain Receptor 1b Enhances Integrin β1-Mediated Cell Migration by Interacting With Talin and Promoting Rac1 Activation.Frontiers in cell and developmental biology · 2022Article
- Discoidin Domain Receptor Tyrosine Kinase 1 (DDR1): A Novel Predictor for Recurrence of Hepatocellular Carcinoma After Curative Resection.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Prognostic and Clinicopathologic Significance of Discoidin Domain Receptors in Different Human Malignancies: A Meta-Analysis.Gastrointestinal tumors · 2021Review
- The Yin and Yang of Discoidin Domain Receptors (DDRs): Implications in Tumor Growth and Metastasis Development.Cancers · 2021Review
Corrections and comments
- Retraction · 2024-09-15Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Euphemisms for Plagiarism · Investigation by Company/Institution · Investigation by Journal/Publisher · Original Data and/or Images not Provided and/or not Available · Paper Mill · Plagiarism of Image · · see also: https://pubpeer.com/publications/183005D064325FAEBE0F9C11201A92
- Retracted
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the function of discoidin domain receptor 1 (DDR1) in hepatocellular carcinoma (HCC) and to further clarify the underlying mechanism.
resultsDDR1 was significantly increased in HCC tissues and cells, which was related to clinical staging and prognosis of HCC. Upregulation of DDR1 promoted EMT and glutamine metabolism in HCC cells, while loss of DDR1 showed the opposite effects. STAT3 bound with the promoter of DDR1, and facilitated the phosphorylation of STAT3. In turn, activation of STAT3 increased the expression of DDR1. Silencing of STAT3 removed the promoting effect of DDR1 on proliferation, migration and invasion of HCC cells. The in vivo tumor growth assay showed that the cross-talk between DDR1 and STAT3 promoted HCC tumorigenesis.
conclusionsOur research revealed the positive feedback of DDR1 and STAT3 promoted EMT and glutamine metabolism in HCC, which provided some experimental basis for clinical treatment or prevention of HCC. MATERIALS AND
methodsThe mRNA expression of DDR1 was detected by qRT-PCR. CCK8 assay, wound healing assay and transwell assay were used to detect the DDR1/ STAT3 function on proliferation, migration and invasion in HCC cells. Western blot was used to calculate protein level of DDR1, STAT3, epithelial-mesenchymal transition (EMT) related proteins.
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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 OpenQuestion graph.