Differential expression of miR-203a-3p in HPV11 and HPV16 infections and its targeting of SOCS3 in keratinocytes

Background: Our study aims to elucidate the differential expression of miR-203a-3p in HPV11 and HPV16 infections and its molecular mechanism of regulating keratinocyte behavior by targeting SOCS3, in order to reveal its role in HPV-related lesions. Methods: Tissue specimens from patients with condyloma acuminata (CA) and healthy controls were collected, and the expression of miR-203a-3p was detected by qRT-PCR. Stable HaCaT cell lines expressing HPV11-E6E7 or HPV16-E6E7 were established. The effects of miR-203a-3p on apoptosis and migration were evaluated. Target genes were screened using an online target prediction program and bioinformatics analysis, and the results were validated using a dual-luciferase reporter assay. Results: miR-203a-3p was significantly downregulated in CA tissues and negatively correlated with viral load (p < 0.05), with a more pronounced downregulation in HPV16-positive samples. Overexpression of miR-203a-3p significantly inhibited HPV-HaCaT cell migration and promoted apoptosis. Transcriptome analysis showed significant differences in pathway enrichment patterns between the two HPV types after miR-203a-3p expression was restored. Furthermore, SOCS3 was identified and validated as a direct functional target of miR-203a-3p. Conclusions: miR-203a-3p is downregulated during HPV infection and targets SOCS3. The miR-203a-3p/SOCS3 pathway exhibits potential regulatory differences between HPV11 and HPV16, thus potentially serving as a therapeutic target for HPV-related lesions.