LOC441178 Overexpression Inhibits the Proliferation and Migration of Esophageal Carcinoma Cells via Methylation of miR-182

Autor:	Congjie Chen, Jiangmu Chen, Zongchi Chen, Weitao Hu, Daxing Cai, Taiyong Fang
Rok vydání:	2020
Předmět:	0301 basic medicine medicine.diagnostic_test Chemistry Bisulfite sequencing Methylation medicine.disease_cause digestive system diseases Flow cytometry 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Oncology Downregulation and upregulation Apoptosis 030220 oncology & carcinogenesis DNA methylation medicine Cancer research Pharmacology (medical) Carcinogenesis Protein kinase B
Zdroj:	OncoTargets and Therapy. 13:11253-11263
ISSN:	1178-6930
DOI:	10.2147/ott.s271711
Popis:	Background Long noncoding RNAs (lncRNAs) have been shown to play an important role in the development and progression of esophageal carcinoma (EC). Recently, lncRNA LOC441178 was shown to be dysregulated in many cancer types; however, the role of LOC441178 in EC remains unclear. Materials and methods Flow cytometry, transwell and wound healing assays were used to measure the apoptosis and migration in esophageal squamous cell carcinoma (ESCC) cells. RT-qPCR was used to detect the level of miR-182 in LOC441178-overexpressed EC cells. In addition, DNA methylation status of miR-182 promoter in LOC441178-overexpressed ESCC cells was detected by methylation-specific PCR (MSP) and bisulfite sequencing PCR. Results In this study, we found that LOC441178 negatively regulated miR-182 expression in ESCC cells. In addition, overexpression of LOC441178 inhibited the proliferation and migration and induced apoptosis in ESCC cells via downregulation of miR-182. Moreover, overexpression of LOC441178 markedly inhibited the phosphorylation of Akt and phosphorylation FOXO3a and increased the expression of FOXO3a in ESCC cells via downregulation of miR-182. Mechanistically, LOC441178 overexpression epigenetically suppressed miR-182 expression via DNA methylation. In vivo experiments revealed that overexpression of LOC441178 inhibited ESCC tumor growth in mouse xenograft model. Conclusion Collectively, our data suggested that LOC441178 overexpression epigenetically inhibited tumorigenesis of ESCC via DNA methylation of miR-182. These data indicated that the LOC441178/miR-182 axis might represent a novel therapeutic option for the treatment of ESCC.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_________::042563e20b8c1363e98af32d680540dd https://doi.org/10.2147/ott.s271711 Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
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