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Updated: Jun 20, 2025

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
Identification of potential therapeutic target SPP1 and related RNA regulatory pathway in keloid based on
Ruxin Xie1, Jiao Yun1, Chenyu Li1
1Department of Burn and Plastic Surgery, West China Hospital of Sichuan University, Chengdu, Sichuan, China.
Objective:
To explore the complex mechanisms of keloid, new approaches have been developed by different strategies. However, conventional treatment did not significantly reduce the recurrence rate. This study aimed to identify new biomarkers and mechanisms for keloid progression through bioinformatics analyses.
Methods:
In our study, microarray datasets for keloid were downloaded from the GEO database. Differentially expressed genes (DEGs) were identified by R software. Multiple bioinformatics tools were used to identify hub genes, and reverse predict upstream miRNAs and lncRNA molecules of target hub genes. Finally, the total RNA-sequencing technique and miRNA microarray were combined to validate the identified genes.
Results:
Thirty-one DEGs were screened out and the upregulated hub gene SPP1 was finally identified, which was consistent with our RNA-sequencing analysis results and validation dataset. In addition, a ceRNA network of mRNA (SPP1)-miRNA (miR-181a-5p)-lncRNA (NEAT1, MALAT1, LINC00667, NORAD, XIST and MIR4458HG) was identified by the bioinformatics databases. The results of our miRNA microarray showed that miR-181a-5p was upregulated in keloid, also we found that the lncRNA NEAT1 could affect keloid progression by retrieving the relevant literature.
Conclusions:
We speculate that SPP1 is a potential candidate biomarker and therapeutic target for patients with keloid, and NEAT1/miR-181a-5p/SPP1 might be the RNA regulatory pathway that regulates keloid formation.
Insights
This study identified SPP1 as a potential biomarker for keloid. The NEAT1/miR-181a-5p/SPP1 pathway may regulate keloid formation, offering new therapeutic targets for this condition.
Area of Science:
- Dermatology and Molecular Biology
- Bioinformatics and Genomics
Background:
- Keloid recurrence rates remain high with conventional treatments.
- Understanding keloid pathogenesis requires novel biomarker and mechanism identification.
Purpose of the Study:
- To identify novel biomarkers and molecular mechanisms underlying keloid progression using bioinformatics.
- To explore potential therapeutic targets for keloid treatment.
Main Methods:
- Downloaded and analyzed microarray datasets from the GEO database for keloid.
- Utilized R software to identify differentially expressed genes (DEGs).
- Employed bioinformatics tools to identify hub genes, predict upstream miRNAs and lncRNAs, and validated findings with RNA-sequencing and miRNA microarray.
Main Results:
- Identified 31 DEGs, with SPP1 identified as a key upregulated hub gene.
- Constructed a ceRNA network involving SPP1 (mRNA), miR-181a-5p (miRNA), and multiple lncRNAs (NEAT1, MALAT1, etc.).
- Confirmed upregulation of miR-181a-5p and identified NEAT1 as a potential regulator of keloid progression.
Conclusions:
- SPP1 is a potential candidate biomarker and therapeutic target for keloid.
- The NEAT1/miR-181a-5p/SPP1 axis represents a potential RNA regulatory pathway in keloid formation.
- Findings provide insights into keloid pathogenesis and suggest avenues for future therapeutic strategies.
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