LAUSR

Abstract Background: We aimed to explore potential molecular basis of keloid formation and response mechanism of keloid to hydrocortisone (HC). Methods: Transcriptional profile of GSE7890 which contained five normal scars with no HC treatment (NNHC), four normal scars treated with HC (NHC), five keloids with no HC treatment (KNHC), and five keloids treated with HC (KHC) samples was downloaded to identify differentially expressed genes (DEGs). Based on DEGs, hierarchical cluster analysis and pathway enrichment analysis were performed. Then, identification of characteristic pathway was performed, followed by calculation of pathway deviation score. Results: Compared to NNHC group, total 1603 DEGs in NHC group, 895 DEGs in KHC group, and 832 DEGs in KNHC group were identified. Hierarchical cluster analysis revealed these four groups could be well distinguished. Total three pathways included cytokine–cytokine receptor interactions were significantly different between KNHC and NNHC groups. Besides, MAPK signaling pathway, endocytosis, and apoptosis were selected between KHC and KNHC groups. Genes of vascular endothelial growth factor C (VEGFC), tenascin C (TNC), and jun proto-oncogene (JUN) were selected as important DEGs in KHC, KNHC, and NHC groups, respectively. Conclusions: VEGF and TNC were, respectively, involved in KHC and KNHC in the mechanism of focal adhesion. JUN might be a potential molecular marker related to normal scar.