FSCN1 binds to lncRNA SNHG20 and regulates proliferation, migration and invasion in hypopharyngeal squamous cell carcinoma

FSCN1 expression was assessed in an HPSCC subset obtained from The Cancer Genome Atlas-Head and Neck Squamous Cell Carcinoma (TCGA-HNSC) dataset. Associations with clinical correlation, pan-cancer expression patterns and immune cell infiltration were evaluated using bioinformatic analysis. The effect of FSCN1 knockdown was investigated in vitro using FaDu cells transfected with FSCN1-targeting siRNA.

Cell proliferation, colony-forming ability, migration and invasion were subsequently assessed. RNA sequencing (RNA-seq) and improved RNA immunoprecipitation sequencing (iRIP-seq) were performed to identify genes associated with FSCN1 expression and RNAs bound by FSCN1. Results: FSCN1 expression was significantly increased in HPSCC tissues.

FSCN1 knockdown inhibited FaDu cell proliferation, colony formation, migration and invasion. RNA-seq identified 2031 differentially expressed genes associated primarily with cell proliferation and apoptosis. iRIP-seq and RNA pull-down indicated an interaction between FSCN1 and lncRNA SNHG20. Furthermore, SNHG20 overexpression partially reversed the suppressive effects of FSCN1 knockdown on the malignant cellular phenotype of FaDu cells and restored the expression of six proliferation_x001E_related genes, such as CDKN1A, IL1A, KRT6A, KRT16, ASCC3, and AKR1C3.

Conclusion: These findings suggest that FSCN1 contributes to HPSCC progression and may exert oncogenic effects, at least in part, through its interaction with SNHG20 and subsequent modulation of downstream gene expression. Nevertheless, the direct regulatory relationship among FSCN1, SNHG20 and these downstream genes requires further experimental validation.