期刊
ONCOTARGETS AND THERAPY
卷 13, 期 -, 页码 4679-4690出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S243215
关键词
ESCC; progression; miR-204-5p; YWHAZ; PI3K/AKT
资金
- National Natural Science Foundation of China [81773129]
- Joint Funds for The Innovation of Science and Technology, Fujian province [2017Y9039, 2018Y9034]
- Program for Innovative Research Team in Science and Technology in Fujian Province University
- Startup Fund for scientific research, Fujian Medical University [2017XQ2027]
Purpose: MicroRNAs dysregulation has been confirmed in multiple malignancies. This paper reported the molecular mechanism of miR-204-5p in esophageal squamous cell carcinoma (ESCC). Methods: miR-204-5p expression in 30 ESCC tumor tissues and 10 normal tissues was downloaded from RNA-seq data. ESCC tissues/normal tissues of 97 ESCC patients were collected. TE-1 and KYSE510 cells were transfected by miR-204-5p mimic, inhibitor, siYWHAZ or their corresponding controls. The phenotype of cells was detected by CCK-8 assay, transwell experiment, and flow cytometry. Luciferase reporter gene assay and RNA-binding protein immunoprecipitation (RIP) were performed to verify the targeting relationship between miR-204-5p and YWHAZ. miR-204-5p and YWHAZ expression in tissues/cells was detected by qRT-PCR and Western blot. Xenograft tumor experiment was performed. Results: miR-204-5p expression was declined in ESCC patients and cells, which was indicated the poor outcome of patients. Compared with siNC group, TE-1 cells in miR-204-5p inhibitor group had higher OD450 value, less cell percentage in G1 phase, and more cell percentage in S phase, lower apoptosis percentage, and higher migration and invasion cell numbers. Moreover, KYSE510 cells of miR-204-5p mimic group showed lower OD450 value, more cell percentage in G1 phase and less cell percentage in S phase, higher apoptosis percentage, and lower migration and invasion cell numbers than control. YWHAZ was directly inhibited by miR-204-5p. Relative to siNC group, TE-1 cells of miR-inhibitor group exhibited higher YWHAZ protein expression, higher OD450 value, less cell percentage in G1 phase and more cell percentage in S phase, lower apoptosis percentage, higher migration and invasion cell numbers, and higher p-PI3K/PI3K and p-AKT/AKT protein expression, while siYWHAZ rescued the effects of miR-inhibitor. miR-204-5p up-regulation inhibited ESCC growth in vivo. Conclusion: miR-204-5p inhibits ESCC progression by targeted inhibition of YWHAZ/PI3K/AKT.
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