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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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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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 |
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author | Guan, Hongya Lv, Pengju Han, Pengli Zhou, Lijuan Liu, Jia Wu, Wei Yan, Ming Xing, Qinghe Cao, Wei |
author_facet | Guan, Hongya Lv, Pengju Han, Pengli Zhou, Lijuan Liu, Jia Wu, Wei Yan, Ming Xing, Qinghe Cao, Wei |
author_sort | Guan, Hongya |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9844631 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-98446312023-01-24 Long non‐coding RNA ESCCAL‐1/miR‐590/LRP6 signaling pathway participates in the progression of esophageal squamous cell carcinoma Guan, Hongya Lv, Pengju Han, Pengli Zhou, Lijuan Liu, Jia Wu, Wei Yan, Ming Xing, Qinghe Cao, Wei Cancer Med RESEARCH ARTICLES 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. John Wiley and Sons Inc. 2022-06-02 /pmc/articles/PMC9844631/ /pubmed/35655441 http://dx.doi.org/10.1002/cam4.4915 Text en © 2022 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | RESEARCH ARTICLES Guan, Hongya Lv, Pengju Han, Pengli Zhou, Lijuan Liu, Jia Wu, Wei Yan, Ming Xing, Qinghe Cao, Wei Long non‐coding RNA ESCCAL‐1/miR‐590/LRP6 signaling pathway participates in the progression of esophageal squamous cell carcinoma |
title | Long non‐coding RNA ESCCAL‐1/miR‐590/LRP6 signaling pathway participates in the progression of esophageal squamous cell carcinoma |
title_full | Long non‐coding RNA ESCCAL‐1/miR‐590/LRP6 signaling pathway participates in the progression of esophageal squamous cell carcinoma |
title_fullStr | Long non‐coding RNA ESCCAL‐1/miR‐590/LRP6 signaling pathway participates in the progression of esophageal squamous cell carcinoma |
title_full_unstemmed | Long non‐coding RNA ESCCAL‐1/miR‐590/LRP6 signaling pathway participates in the progression of esophageal squamous cell carcinoma |
title_short | Long non‐coding RNA ESCCAL‐1/miR‐590/LRP6 signaling pathway participates in the progression of esophageal squamous cell carcinoma |
title_sort | long non‐coding rna esccal‐1/mir‐590/lrp6 signaling pathway participates in the progression of esophageal squamous cell carcinoma |
topic | RESEARCH ARTICLES |
url | 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 |
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