HCG11 inhibits salivary adenoid cystic carcinoma by upregulating EphA2 via binding to miR-1297

Objective. Ephrin receptor A2 (EphA2) was reported to be related to the tumorigenesis of salivary adenoid cystic carcinoma (SACC), which is a rare malignancy accounting for less than 1% of all oral and maxillofacial tumors. This research aimed to assess the molecular mechanisms of EphA2 in SACC.Study Design. The expression of long non-coding RNA human leukocyte antigen complex group 11 (HCG11), microRNA-1297 (miR-1297), and EphA2 in SACC cell lines compared with normal human salivary gland (HSG) cell line was measured by reverse transcription-quantitative polymerase chain reaction. EphA2 protein level was detected by western blot. 5-ethynyl-2'-deoxyuri-dine (EdU), colony formation, Transwell, and wounding healing experiments were applied to evaluate SACC cell proliferation, migration, and invasion. The relationship among HCG11, miR-1297, and EphA2 was confirmed by luciferase reporter, RNA pull-down, and RNA immunoprecipitation experiments.Results. HCG11 and EphA2 were downregulated while miR-1297 was upregulated in SACC cells. EphA2 overexpression sup-pressed SACC cell proliferation, migration, and invasion. HCG11 bound to miR-1297 to reduce the inhibition of miR-1297 on EphA2 expression. EphA2 knockdown reversed the suppression of HCG11 overexpression on SACC cell phenotypes.Conclusion. This study identified the HCG11/miR-1297/EphA2 regulatory axis in SACC, which might provide novel therapeutic targets for SACC. (Oral Surg Oral Med Oral Pathol Oral Radiol 2023;135:257-267)

Automated summary

This study identified the regulatory axis of HCG11/miR-1297/EphA2 in SACC, which may provide novel therapeutic targets for SACC.