Zhiqun Li1, Xiaoliu Zhou1, Jiajun Huang1, Zhencai Xu1, Chengliang Xing1, Junwei Yang1, Xuejun Zhou2. 1. Department of Otolaryngology Head and Neck Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou, 570102, Hainan, China. 2. Department of Otolaryngology Head and Neck Surgery, The First Affiliated Hospital of Hainan Medical University, Haikou, 570102, Hainan, China. Electronic address: xuejunzhou65@163.com.
Abstract
BACKGROUND: Nasopharyngeal 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. METHODS: The 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. RESULTS: The 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. CONCLUSIONS: We 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.
BACKGROUND: Nasopharyngeal 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. METHODS: The 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. RESULTS: The 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. CONCLUSIONS: We 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.