Y-H Liu1, J-L Liu, Z Wang, X-H Zhu, X-B Chen, M-Q Wang. 1. Department of Otorhinolaryngology Head and Neck Surgery, Second Affiliated Hospital of Nanchang University, Nanchang, P.R. China. liuyh_ncu@163.com.
Abstract
OBJECTIVE: Mounting evidence has suggested that microRNAs (miRNAs) play crucial roles in the progression of nasopharyngeal carcinoma (NPC). However, the molecular mechanism remains not fully understood. We aimed to examine the expression and biological function of miR-122-5p in NPC. MATERIALS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction was conducted to examine the expression of miR-122-5p. Cell Counting Kit-8 assay, colony formation assay, wound healing assay and transwell assay were performed to measure cell proliferation, colony formation, migration and invasion. Luciferase reporter assay and Western blot assay were used to confirm the target gene of miR-122-5p. RESULTS: The results showed that miR-122-5p was significantly downregulated in NPC cell lines. Additionally, it was demonstrated that special AT-rich sequence-binding protein 1 (SATB1) was targeted by miR-122-5p. Furthermore, our results revealed that miR-122-5p inhibits cell proliferation, colony formation, cell migration and cell invasion by targeting SATB1. CONCLUSIONS: Our data suggested that miR-122-5p functions as a tumor suppressor and may be a therapeutic target for NPC.
OBJECTIVE: Mounting evidence has suggested that microRNAs (miRNAs) play crucial roles in the progression of nasopharyngeal carcinoma (NPC). However, the molecular mechanism remains not fully understood. We aimed to examine the expression and biological function of miR-122-5p in NPC. MATERIALS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction was conducted to examine the expression of miR-122-5p. Cell Counting Kit-8 assay, colony formation assay, wound healing assay and transwell assay were performed to measure cell proliferation, colony formation, migration and invasion. Luciferase reporter assay and Western blot assay were used to confirm the target gene of miR-122-5p. RESULTS: The results showed that miR-122-5p was significantly downregulated in NPC cell lines. Additionally, it was demonstrated that special AT-rich sequence-binding protein 1 (SATB1) was targeted by miR-122-5p. Furthermore, our results revealed that miR-122-5p inhibits cell proliferation, colony formation, cell migration and cell invasion by targeting SATB1. CONCLUSIONS: Our data suggested that miR-122-5p functions as a tumor suppressor and may be a therapeutic target for NPC.