CEMIP induces TGF-β/Smad signaling to promote keloid development by binding to SPARC.
| Autor: | Li X; Department of Plastic Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, China., Zhang W; Department of Plastic Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, China., Li X; Department of Plastic Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, China. Electronic address: Lixiaojing930111@163.com. |
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| Jazyk: | angličtina |
| Zdroj: | Clinics (Sao Paulo, Brazil) [Clinics (Sao Paulo)] 2024 Oct 29; Vol. 79, pp. 100523. Date of Electronic Publication: 2024 Oct 29 (Print Publication: 2024). |
| DOI: | 10.1016/j.clinsp.2024.100523 |
| Abstrakt: | Background: Cell Migration Inducing Hyaluronidase 1 (CEMIP) is a protein that plays regulatory functions in a variety of cellular processes in many diseases. Nevertheless, its role and molecular mechanism in keloid hyperplasia are still elusive. Methods: Expressions of CEMIP and Secreted Protein acidic and Rich in Cysteine (SPARC) were detected by qRT-PCR and western blot. CCK-8 assay, along with immunofluorescence staining, was applied for the assessment of cell proliferation. The capabilities of cells to migrate and invade were evaluated utilizing wound healing and Transwell, while Extracellular Matrix (ECM) deposition was measured by immunofluorescence and western blot. The interaction of CEMIP and SPARC was predicted by the Coexpedia and PPA-red databases and verified by co-IP. Western blot was adopted for the estimation of TGF-β/Smad pathway-related proteins. Results: The data demonstrated that CEMIP expression was elevated in Keloid Fibroblasts (KF). CEMIP interference suppressed cell proliferative, migrative and invasive capabilities and ECM deposition in KF. Mechanistically, bioinformatics analysis revealed that CEMIP was co-expressed with SPARC and CEMIP protein could bind to SPARC. SPARC expression was reduced in CEMIP-silenced cells. SPARC overexpression counteracted the impacts of CEMIP silencing on cell proliferative, migrative and invasive capabilities and ECM deposition in KF. In addition, the expressions of TGF-β/Smad signaling-related proteins were decreased by CEMIP silencing via the inhibition of SPARC. Conclusion: In summary, this study revealed that CEMIP modulated KF proliferation, migration, invasion and ECM deposition by TGF-β/Smad signaling through binding to SPARC. Competing Interests: Declaration of competing interest The authors declare no conflicts of interest. (Copyright © 2024. Published by Elsevier España, S.L.U.) |
| Databáze: | MEDLINE |
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