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MiR‐671‐5p sponging activity of circMMP1 promotes esophageal squamous cancer progression
BACKGROUND: The aim of this study was to explore the function and mechanism of circular RNA (circRNA) matrix metallopeptidase 1 (circMMP1) in the progression of esophageal squamous cell carcinoma (ESCC). METHODS: CircMMP1 expression was detected by quantitative real‐time PCR (qRT‐PCR), and its relat...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons Australia, Ltd
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10569906/ https://www.ncbi.nlm.nih.gov/pubmed/37635445 http://dx.doi.org/10.1111/1759-7714.15078 |
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author | Li, Rong Chai, Linyan Lei, Lei Guo, Rong Wen, Xiulin |
author_facet | Li, Rong Chai, Linyan Lei, Lei Guo, Rong Wen, Xiulin |
author_sort | Li, Rong |
collection | PubMed |
description | BACKGROUND: The aim of this study was to explore the function and mechanism of circular RNA (circRNA) matrix metallopeptidase 1 (circMMP1) in the progression of esophageal squamous cell carcinoma (ESCC). METHODS: CircMMP1 expression was detected by quantitative real‐time PCR (qRT‐PCR), and its relationship with the prognosis of ESCC patients was evaluated by Kaplan–Meier analysis. Cells were transfected using corresponding plasmids, and the cell proliferation activity, migration and invasion capabilities in vitro were assessed. The protein level in tissues and cells was analyzed using western blotting. RNA pulldown, dual‐luciferase reporter assay and RNA immunoprecipitation assay were performed in ESCC cells to detect the interaction between circMMP1 and miR‐671‐5p, or the correlation between miR‐671‐5p and ANO1. Xenograft tumor experiment was carried out to uncover the function of circMMP1 in vivo. RESULTS: The high level of circMMP1 in tumor tissues was associated with poor prognoses of ESCC patients. Knockdown of circMMP1 suppressed ESCC cell proliferation, migration and invasion in vitro. MiR‐671‐5p was the target of circMMP1 and mediated the inhibition effect of circMMP1 on ESCC cells. CircMMP1 targeted miR‐671‐5p to regulate ANO1 expression, which was downstream of miR‐671‐5p. Overexpression of ANO1 weakened tumor‐repressive function of circMMP1 knockdown in ESCC cells. Moreover, silencing of circMMP1 impeded ESCC tumor growth in vivo. CONCLUSION: Our study provided novel evidence that circMMP1 accelerated ESCC progression by acting as a miR‐671‐5p sponge to enhance ANO1 expression. |
format | Online Article Text |
id | pubmed-10569906 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley & Sons Australia, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-105699062023-10-13 MiR‐671‐5p sponging activity of circMMP1 promotes esophageal squamous cancer progression Li, Rong Chai, Linyan Lei, Lei Guo, Rong Wen, Xiulin Thorac Cancer Original Articles BACKGROUND: The aim of this study was to explore the function and mechanism of circular RNA (circRNA) matrix metallopeptidase 1 (circMMP1) in the progression of esophageal squamous cell carcinoma (ESCC). METHODS: CircMMP1 expression was detected by quantitative real‐time PCR (qRT‐PCR), and its relationship with the prognosis of ESCC patients was evaluated by Kaplan–Meier analysis. Cells were transfected using corresponding plasmids, and the cell proliferation activity, migration and invasion capabilities in vitro were assessed. The protein level in tissues and cells was analyzed using western blotting. RNA pulldown, dual‐luciferase reporter assay and RNA immunoprecipitation assay were performed in ESCC cells to detect the interaction between circMMP1 and miR‐671‐5p, or the correlation between miR‐671‐5p and ANO1. Xenograft tumor experiment was carried out to uncover the function of circMMP1 in vivo. RESULTS: The high level of circMMP1 in tumor tissues was associated with poor prognoses of ESCC patients. Knockdown of circMMP1 suppressed ESCC cell proliferation, migration and invasion in vitro. MiR‐671‐5p was the target of circMMP1 and mediated the inhibition effect of circMMP1 on ESCC cells. CircMMP1 targeted miR‐671‐5p to regulate ANO1 expression, which was downstream of miR‐671‐5p. Overexpression of ANO1 weakened tumor‐repressive function of circMMP1 knockdown in ESCC cells. Moreover, silencing of circMMP1 impeded ESCC tumor growth in vivo. CONCLUSION: Our study provided novel evidence that circMMP1 accelerated ESCC progression by acting as a miR‐671‐5p sponge to enhance ANO1 expression. John Wiley & Sons Australia, Ltd 2023-08-27 /pmc/articles/PMC10569906/ /pubmed/37635445 http://dx.doi.org/10.1111/1759-7714.15078 Text en © 2023 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Li, Rong Chai, Linyan Lei, Lei Guo, Rong Wen, Xiulin MiR‐671‐5p sponging activity of circMMP1 promotes esophageal squamous cancer progression |
title |
MiR‐671‐5p sponging activity of circMMP1 promotes esophageal squamous cancer progression |
title_full |
MiR‐671‐5p sponging activity of circMMP1 promotes esophageal squamous cancer progression |
title_fullStr |
MiR‐671‐5p sponging activity of circMMP1 promotes esophageal squamous cancer progression |
title_full_unstemmed |
MiR‐671‐5p sponging activity of circMMP1 promotes esophageal squamous cancer progression |
title_short |
MiR‐671‐5p sponging activity of circMMP1 promotes esophageal squamous cancer progression |
title_sort | mir‐671‐5p sponging activity of circmmp1 promotes esophageal squamous cancer progression |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10569906/ https://www.ncbi.nlm.nih.gov/pubmed/37635445 http://dx.doi.org/10.1111/1759-7714.15078 |
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