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Long non‐coding RNA ESCCAL‐1/miR‐590/LRP6 signaling pathway participates in the progression of esophageal squamous cell carcinoma

BACKGROUND: Long non‐coding RNAs (lncRNAs) have critical functions within esophageal squamous cell carcinoma (ESCC). However, the function and mechanism underlying ESCC‐associated lncRNA‐1 (ESCCAL‐1) in ESCC tumorigenesis have not been well clarified. METHODS: ESCCAL‐1, miR‐590 and LRP6 were quantif...

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Detalles Bibliográficos
Autores principales: Guan, Hongya, Lv, Pengju, Han, Pengli, Zhou, Lijuan, Liu, Jia, Wu, Wei, Yan, Ming, Xing, Qinghe, Cao, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9844631/
https://www.ncbi.nlm.nih.gov/pubmed/35655441
http://dx.doi.org/10.1002/cam4.4915
Descripción
Sumario:BACKGROUND: Long non‐coding RNAs (lncRNAs) have critical functions within esophageal squamous cell carcinoma (ESCC). However, the function and mechanism underlying ESCC‐associated lncRNA‐1 (ESCCAL‐1) in ESCC tumorigenesis have not been well clarified. METHODS: ESCCAL‐1, miR‐590 and LRP6 were quantified using qRT‐PCR. Cell viability, migration and invasion abilities were measured using CCK‐8 assay and transwell assays. The protein pression was determined with western blot assay. The xenograft model assays were used to examine the impact of ESCCAL‐1 on tumorigenic effect in vivo. Direct relationships among ESCCAL‐1, miR‐590 and LRP6 were confirmed using dual‐luciferase reporter assays. RESULTS: The present work discovered the ESCCAL‐1 up‐regulation within ESCC. Furthermore, ESCCAL‐1 was found to interact with miR‐590 and consequently restrict its expression. Functionally, knocking down ESCCAL‐1 or over‐expressing miR‐590 hindered ESCC cell growth, invasion, and migration in vitro. Moreover, inhibition of miR‐590 could reverse the effect of knockdown of ESCCAL‐1 on cells. Importantly, it was confirmed that LRP6 was miR‐590’s downstream target and LRP6 over‐expression also partly abolished the role of miR‐590 overexpression in ESCC cells. CONCLUSION: We have uncovered a novel regulatory network comprising aberrant interaction of ESCCAL‐1/miR‐590/LRP6 participated in ESCC progression.