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While many gene expression studies have focused on male pattern baldness (MPB), few studies have investigated the genetic differences between bald and non-bald hair follicles in female pattern hair loss (FPHL). This study aimed to identify molecular biomarkers associated with FPHL through genetic analysis of paired bald and non-bald hair follicles from 18 FPHL patients, using next-generation sequencing (NGS) techniques. RNA transcriptome analysis was performed to identify differentially expressed genes (DEGs) between bald and non-bald hair follicles in FPHL. The DEGs were validated using real-time PCR, and protein expression was confirmed through immunohistochemistry and western blot analysis. Our findings suggest that HOXB13, SFRP2, PTGDS, CXCR3, SFRP4, SOD3, and DCN are significantly upregulated in bald hair follicles compared to non-bald hair follicles in FPHL. SFRP2 and PTGDS were found to be consistently highly expressed in bald hair follicles in all 18 samples. Additionally, elevated protein levels of SFRP2 and PTGDS were confirmed through western blot and immunohistochemical analysis. Our study identified SFRP2 and PTGDS as potential biomarkers for FPHL and suggests that they may play a role in inducing hair loss in this condition. These findings provide a foundation for further research on the pathogenesis of FPHL and potential therapeutic targets. [ABSTRACT FROM AUTHOR]

Background: Many candidate genes for androgenetic alopecia (AGA) have been identified in studies of the Caucasians and some Asian populations. Aims: This study aimed to confirm the known susceptibility genes reported in previous studies and find additional candidate genes for high‐risk individuals for AGA in Korean population. Patients/Methods: We recapitulated the previously reported SNPs and identified the novel Korean AGA risk genetic variants using a Korean hospital‐based AGA case and control samples. The population was consisting of 494 individuals (275 AGA cases and 146 controls). Using the 800 K SNPs of precision medical research array (PMRA SNP microarray chip) and imputation‐based SNPs, 12 previous GWAS reports for AGA and a total of 62 160 SNPs were examined in our study samples. Also, we conducted the genome‐wide association study (GWAS) by the logistic regression analyses for AGA cases and controls with controlling the age as the covariates. Results: Among the 62 160 SNPs, a total of 1143 SNPs in 76 gene regions showed weak replication tendency with the p‐values <0.05 and same direction of effects. Additionally, the GWAS results showed 110 SNPs in 13 independent regions with the suggestive p‐values <1.00 × 10−5. The most significantly replicated SNP resided on chromosome 20, which were similar to other AGA replication studies including Chinese study. The GWAS identified two SNPs (rs11010734 and rs2420640) increasing the risk for AGA in our study population. Conclusions: Our study would be a reference of the non‐European studies to better understand AGA in different populations and ancestral contexts. [ABSTRACT FROM AUTHOR]

Background The exact physiological function of REIC/Dkk-3 in the development of squamous cell carcinoma(SCC) remains unclear. Objective We aimed to investigate the expression pattern and functional role of REIC/Dkk-3 in the development of SCC. Methods We stained normal skin, actinic keratosis (AK) and SCC tissue with REIC/Dkk-3. The proliferation and migration of SCC 12 over-expressed with REIC/Dkk-3 were observed. For in vivo study, SCC12 cells in PBS, SCC12 cells containing LacZ, and REIC/Dkk-3-transduced SCC 12 cells were injected intra-dermally into the left and right backside flanks of SCID mice respectively, and tumor growth was evaluated. Results REIC/Dkk-3 staining was detected throughout the full epidermis in normal skin, focally positive in AK. Negative or very low stain of REIC/Dkk-3 was observed in SCC in situ, keratoacanthoma, and SCC. REIC/Dkk-3 mRNA level in SCC was very low compared with that in normal skin tissue. REIC/Dkk-3 significantly decreased the proliferation and migration of SCC12 cells comparing with control (p < 0.05). Cyclin D1 and CDK4/6 expression was slightly lower and p21 was very higher in REIC/Dkk-3-overexpressed group than in the LacZ group. Fewer ITGA6 cells were found in the REIC/Dkk-3 overexpressed group than in the LacZ control (p < 0.01). Mean tumor volume was smallest in the REIC/Dkk-3 overexpressed group (p < 0.01) 21 days after the intradermal injection of SCC12 cells. Conclusion REIC/Dkk-3 could be involved early in SCC development and have inhibitory effect on the development of SCC. [ABSTRACT FROM AUTHOR]