• Zhiqun Li, Xiaoliu Zhou, Jiajun Huang, Zhencai Xu, Chengliang Xing, Junwei Yang, and Xuejun Zhou.
• Department of Otolaryngology Head and Neck Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou, 570102, Hainan, China.
• Am. J. Med. Sci. 2022 Jun 16.

BackgroundNasopharyngeal cancer (NPC) is a rare cancer type with a low five-year survival rate. Dysregulation of PYCR1 and miR-150-5p has been involved in the development of various cancers. However, the molecular mechanism of the miR-150-5p-PYCR1 axis in NPC remains unclear.MethodsThe expressions of miR-150-5p and PYCR1 in NPC tissues and cells were measured by RT-qPCR. The luciferase assay and RNA pull-down assay were used to confirm the interaction between miR-150-5p and PYCR1. The function of overexpression of miR-150-5p and PYCR1 were detected by cell viability, proliferation, migration and invasion in NPC C666-1 and SUNE-1 cells.ResultsThe miR-150-5p expression was reduced in NPC tissues and cells and negatively correlated with PYCR1 level. Upregulation of miR-150-5p conspicuously repressed cell growth. However, upregulation of PYCR1 significantly facilitated the development of NPC, which further suppressed NPC tumorigenesis by abolishing the effect of miR-150-5p.ConclusionsWe clarified that miR-150-5p attenuated NPC tumorigenesis through reducing PYCR1 expression. This provides a new perspective of NPC involving both miR-150-5p and PYCR1 for the treatment of NPC.Copyright © 2022. Published by Elsevier Inc.

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