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′-deoxyuridine
(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 pulldown, and
RNA immunoprecipitation experiments.
Results
HCG11 and EphA2 were downregulated while miR-1297 was upregulated in SACC cells. EphA2
overexpression suppressed 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.
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Article info
Publication history
Published online: September 06, 2022
Accepted:
August 28,
2022
Received in revised form:
August 4,
2022
Received:
April 1,
2022
Identification
Copyright
© 2022 Elsevier Inc. All rights reserved.