MicroRNA-383-5p inhibits the progression of gastric carcinoma via targeting HDAC9 expression
AUTOR(ES)
Xu, Gang
FONTE
Braz J Med Biol Res
DATA DE PUBLICAÇÃO
29/07/2019
RESUMO
MicroRNAs (miRNAs), as post-transcriptional regulators, have been reported to be involved in the initiation and progression of various types of cancer, including gastric cancer (GC). The present study aimed to investigate the role of miR-383-5p in gastric carcinogenesis. Cell viability was analyzed using CCK-8 kit. Annexin V-fluorescein isothiocyanate/propidium iodide double staining was used to evaluate cell apoptosis. The expression levels of miR-383-5p and histone deacetylase 9 (HDAC9) mRNA in GC tissues and cell lines were analyzed using RT-qPCR. The protein expression of HDAC9 was detected by western blotting. We found that HDAC9 was up-regulated and miR-383-5p was down-regulated in GC tissues and cell lines. High HDAC9 expression or low miR-383-5p expression was closely related to poor prognosis and metastasis in GC patients. HDAC9 knockout or miR-383-5p mimics led to growth inhibition and increased apoptosis in AGS and SGC-7901 cells. More importantly, we validated that miR-383-5p as a post-transcriptional regulator inhibited HDAC9 expression and was inversely correlated with HDAC9 expression in GC tissues. miR-383-5p had the opposite effects to HDAC9 in gastric carcinogenesis. miR-383-5p played an important role in gastric carcinogenesis, and it is one of the important mechanisms to regulate oncogenic HDAC9 in GC, which might be helpful in the development of novel therapeutic strategies for the treatment of GC.
Documentos Relacionados
- MicroRNA-375 inhibits laryngeal squamous cell carcinoma progression via targeting CST1
- MicroRNA-340-5p modulates cisplatin resistance by targeting LPAATβ in osteosarcoma
- MicroRNA-451a, microRNA-34a-5p, and microRNA-221-3p as predictors of response to antidepressant treatment
- MicroRNA control of PHABULOSA in leaf development: importance of pairing to the microRNA 5′ region
- Cloning and characterization of a histone deacetylase, HDAC9