ReviewOncology research2025
Research progress on the role of decorin in the development of oral mucosal carcinogenesis.
Review in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The role of exercise-induced myokines in cancer-associated inflammation and immune regulation: mechanisms and prospects.Frontiers in sports and active living · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decorin (DCN) is primarily found in the connective tissues of various parts of the body, including the lungs, kidneys, bone tissue, aorta, and tendons. It is an important component of the extracellular matrix (ECM) and belongs to the class I small leucine-rich proteoglycans family. DCN is increasingly attracting attention due to its significant role in tumors, fibrotic diseases, and the regulation of vascular formation. Moreover, its anti-tumor properties have positioned it as a promising biomarker in the fight against cancer. Numerous studies have confirmed that DCN can exert inhibitory effects in various solid tumors, particularly in oral squamous cell carcinoma (OSCC), by activating its downstream pathways through binding with the epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition (MET) receptor, or by stabilizing and enhancing the expression of the tumor suppressor gene p53 to mediate apoptosis in cancer cells that have undergone mutation. The occurrence of OSCC is a continuous and dynamic process, encompassing the transition from normal mucosa to oral potentially malignant disorders (OPMDs), and further progressing from OPMDs to the malignant transformation into OSCC. We have found that DCN may exhibit a bidirectional effect in the progression of oral mucosal carcinogenesis, showing a trend of initial elevation followed by a decline, which decreases with the differentiation of OSCC. In OPMDs, DCN exhibits high expression and may be associated with malignant transformation, possibly linked to the increased expression of P53 in OPMDs. In OSCC, the expression of DCN is reduced, which can impact OSCC angiogenesis, and inhibit tumor cell proliferation, migration, and invasion capabilities, serving as a potential marker for predicting adverse prognosis in OSCC patients. This article reviews the current research status of DCN, covering its molecular structure, properties, and involvement in the onset and progression of oral mucosal carcinogenesis. It elucidates DCN's role in this process and aims to offer insights for future investigations into its mechanism of action in oral mucosal carcinogenesis and its potential application in the early diagnosis and treatment of OSCC.
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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.