Inhibin A contributes to the tumorigenesis of oral squamous cell carcinoma by KIAA1429‐mediated m6A modification

Abstract

AbstractBackgroundInhibin A and N6‐methyladenosine methylation modifications participate in oral squamous cell carcinoma development. However, the N6‐methyladenosine modification of Inhibin A in oral squamous cell carcinoma has not been revealed. This study reveals a key gene “Inhibin A” that may affect the tumorigenesis of oral squamous cell carcinoma and its molecular mechanisms on N6‐methyladenosine methyltransferase KIAA1429‐mediated N6‐methyladenosine methylation modification.MethodsBioinformatics analysis and quantitative real‐time polymerase chain reaction identified the potential regulatory genes in oral squamous cell carcinoma. We examined the changes in the proliferation (Cell Counting Kit‐8 assay), migration (transwell migration assay), and invasion (transwell invasion assays) of oral squamous cell carcinoma cells. We performed a xenograft tumor experiment to validate the role of Inhibin A in oral squamous cell carcinoma in vivo. The interactions between Inhibin A and KIAA1429 were analyzed using bioinformatics, methylated RNA immunoprecipitation‐qPCR, quantitative real‐time polymerase chain reaction, and Western blotting experiments.ResultsInhibin A had the highest expression in patients with oral squamous cell carcinoma. Inhibin A silencing impaired the ability of oral squamous cell carcinoma cells to proliferate, migrate, and invade, as well as limited the tumorous growth of oral squamous cell carcinoma cells in vivo. Bioinformatics analysis showed that Inhibin A expression positively interacted with KIAA1429 expression in The Cancer Genome Atlas database. The levels were also upregulated in our clinical samples. Furthermore, KIAA1429 silencing repressed the N6‐methyladenosine level of Inhibin A in oral squamous cell carcinoma.ConclusionsInhibin A promotes the tumorigenesis of oral squamous cell carcinoma by KIAA1429‐mediated N6‐methyladenosine modification. This study adds to our current knowledge of the molecular mechanisms underlying oral squamous cell carcinoma malignancy.