HAGLROS knockdown restrained cell proliferation, migration and invasion and facilitated apoptosis in laryngeal cancer via miR-138-5p/CLN5 axis.

BACKGROUND

This work investigated the role of HAGLROS in laryngeal cancer (LC).

METHODS

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.

RESULTS

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.

CONCLUSION

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.