Abstract
Laryngeal cancer accounts for 25%–30% of tumors in the head and neck. Cystatin SN (CST1) was revealed to show upregulated expression in this cancer, while its functions and upstream pathway remain unknown and need investigation. The current study was designed to solve this problem. We designed short hairpin RNAs targeting CST1 for the loss-of-function assays to probe the influences of CST1 in laryngeal cancer cell proliferation and motility. The upstream competitive endogenous RNA pattern of CST1 was searched using bioinformatics analysis and confirmed by luciferase reporter assays. The experimental results demonstrated that CST1 is a tumor facilitator in laryngeal cancer by stimulating cellular proliferative, migrative, and invasive abilities. CST1 is regulated by the long intergenic non-protein-coding RNA 1278 (LINC01278)/miR-185-5p axis. LINC01278 knockdown and miR-185-5p overexpression exert the same functions as CST1 knockdown to repress cancer cell proliferation, migration, and invasion. In conclusion, LINC01278 plays an oncogenic role in laryngeal cancer by suppressing miR-185-5p to enhance CST1 expression, which enriches the molecular mechanism for the carcinogenesis of laryngeal cancer.
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