Hsa-mir-1293/GLI1/PTCH1 axis is involved in proliferation, migration, and EMT of laryngeal cancer

This study aimed to investigate the specific role and molecular mechanisms of the transcription factor GLI1 and its upstream regulatory miRNA, hsa-mir-1293, in laryngeal cancer development, with a focus on elucidating the function of the hsa-mir-1293/GLI1/PTCH1 signaling axis in regulating laryngeal cancer cell proliferation, migration, and EMT.

Differentially expressed miRNAs were screened from TCGA laryngeal cancer miRNA data, and the interaction between hsa-mir-1293 and GLI1 was validated using a dual luciferase reporter assay. The effects of hsa-mir-1293 on TU212 cell proliferation, clonal formation, and invasion were examined. The role of GLI1's downstream target, PTCH1, in cell proliferation, migration, and EMT was further investigated.

Bioinformatics analysis identified hsa-mir-1293 as the most significantly down-regulated miRNA in laryngeal carcinoma, showing a negative correlation with GLI1 expression. Overexpression of hsa-mir-1293 suppressed TU212 cell proliferation, clonal formation, and invasion. Silencing GLI1 reduced PTCH1 expression, while PTCH1 overexpression promoted cell invasion, migration, and EMT.

Hsa-mir-1293 targets GLI1, and the GLI1/PTCH1 axis plays a critical role in laryngeal cancer cell proliferation, migration, and EMT.