This work investigated the role of HAGLROS in laryngeal cancer (LC). HAGLROS expression in the head and neck squamous cell carcinoma (HNSC), target miRNAs of HAGLROS, target mRNAs of miR-138-5p, and the binding sites of HAGLROS and miR-138-5p or CLN5 and miR-138-5p were predicted through bioinformatics. HAGLROS, miR-138-5p, CLN5, Bcl-2, and Bax levels were detected by qRT-PCR and Western blot. The biological functions of LC cells were assessed through CCK-8, colony formation assays, transwell assay, and flow cytometry assay. The targeting relationship between HAGLROS and miR-138-5p or CLN5 and miR-138-5p was confirmed by dual luciferase gene reporter analysis. HAGLROS was upregulated in LC. HAGLROS-specific small interfering RNA (Si-HAGLROS) inhibited the viability, proliferation, migration, and invasion while increased the apoptosis in LC cells. MiR-138-5p was a target of HAGLROS and the miR-138-5p inhibitor reversed the effects of si-HAGLROS on LC cells. CLN5 was a target of miR-138-5p. MiR-138-5p inhibitor raised the viability, migration and invasion, and Bcl-2 expression while declined Bax expression in LC cells, with si-CLN5 performing the opposite effects and reversing the effects of miR-138-5p inhibitor. Silenced HAGLROS restrained the LC cells' abilities to proliferate, migrate, and invade as well as facilitated apoptosis in LC via miR-138-5p/CLN5 axis.