MALAT1 and head and neck squamous cell carcinoma: In the meanwhile, we found the phosphorylation of P65 at Ser536 and β-catenin at Ser675, the key amino acid residues for the activation of these two pathways [24, 25], was inhibited by MALAT1 depletion, which further suggested that MALAT1 could activate P65 and β-catenin to promote HNSCC progression.