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Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer

PURPOSE: The long noncoding RNA C1QTNF1 antisense RNA 1 (C1QTNF1-AS1) contributes to hepatocellular carcinoma development. However, its expression and roles in colorectal cancer (CRC) have not been fully explored. Therefore, this study determined the expression and roles of C1QTNF1-AS1 in CRC and el...

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Autores principales: Jin, Shifeng, Liu, Yi, Wang, Wenjing, Li, Ze
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7700093/
https://www.ncbi.nlm.nih.gov/pubmed/33262654
http://dx.doi.org/10.2147/CMAR.S262096
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author Jin, Shifeng
Liu, Yi
Wang, Wenjing
Li, Ze
author_facet Jin, Shifeng
Liu, Yi
Wang, Wenjing
Li, Ze
author_sort Jin, Shifeng
collection PubMed
description PURPOSE: The long noncoding RNA C1QTNF1 antisense RNA 1 (C1QTNF1-AS1) contributes to hepatocellular carcinoma development. However, its expression and roles in colorectal cancer (CRC) have not been fully explored. Therefore, this study determined the expression and roles of C1QTNF1-AS1 in CRC and elucidated its detailed mechanism of action. METHODS: C1QTNF1-AS1 expression in CRC tissues and cell lines was assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). We used Cell Counting Kit-8, flow cytometry, cell migration and invasion assays, and a xenograft tumor model to test the effects of C1QTNF1-AS1 on CRC malignancy. The associations among C1QTNF1-AS1, microRNA-484 (miR-484), and hexokinase 2 (HK2) were explored using luciferase reporter assay, RNA immunoprecipitation, RT–qPCR, and Western blotting. RESULTS: C1QTNF1-AS1 was overexpressed in CRC and related to poor prognosis. C1QTNF1-AS1 interference inhibited CRC cell proliferation, migration, and invasion but induced apoptosis. Furthermore, C1QTNF1-AS1 deficiency impaired tumor growth in vivo. Mechanistically, C1QTNF1-AS1 adsorbed miR-484, thereby increasing the expression of its target HK2. Rescue experiments revealed that the effects of C1QTNF1-AS1 deficiency in CRC cells were reversed by inhibiting miR-484 or upregulating HK2. CONCLUSION: C1QTNF1-AS1 drives CRC progression by sponging miR-484 and consequently upregulating HK2. The C1QTNF1-AS1/miR-484/HK2 pathway may serve as a diagnostic and therapeutic target for CRC.
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spelling pubmed-77000932020-11-30 Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer Jin, Shifeng Liu, Yi Wang, Wenjing Li, Ze Cancer Manag Res Original Research PURPOSE: The long noncoding RNA C1QTNF1 antisense RNA 1 (C1QTNF1-AS1) contributes to hepatocellular carcinoma development. However, its expression and roles in colorectal cancer (CRC) have not been fully explored. Therefore, this study determined the expression and roles of C1QTNF1-AS1 in CRC and elucidated its detailed mechanism of action. METHODS: C1QTNF1-AS1 expression in CRC tissues and cell lines was assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). We used Cell Counting Kit-8, flow cytometry, cell migration and invasion assays, and a xenograft tumor model to test the effects of C1QTNF1-AS1 on CRC malignancy. The associations among C1QTNF1-AS1, microRNA-484 (miR-484), and hexokinase 2 (HK2) were explored using luciferase reporter assay, RNA immunoprecipitation, RT–qPCR, and Western blotting. RESULTS: C1QTNF1-AS1 was overexpressed in CRC and related to poor prognosis. C1QTNF1-AS1 interference inhibited CRC cell proliferation, migration, and invasion but induced apoptosis. Furthermore, C1QTNF1-AS1 deficiency impaired tumor growth in vivo. Mechanistically, C1QTNF1-AS1 adsorbed miR-484, thereby increasing the expression of its target HK2. Rescue experiments revealed that the effects of C1QTNF1-AS1 deficiency in CRC cells were reversed by inhibiting miR-484 or upregulating HK2. CONCLUSION: C1QTNF1-AS1 drives CRC progression by sponging miR-484 and consequently upregulating HK2. The C1QTNF1-AS1/miR-484/HK2 pathway may serve as a diagnostic and therapeutic target for CRC. Dove 2020-11-24 /pmc/articles/PMC7700093/ /pubmed/33262654 http://dx.doi.org/10.2147/CMAR.S262096 Text en © 2020 Jin et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Jin, Shifeng
Liu, Yi
Wang, Wenjing
Li, Ze
Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer
title Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer
title_full Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer
title_fullStr Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer
title_full_unstemmed Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer
title_short Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer
title_sort long non-coding rna c1qtnf1 antisense rna 1 upregulates hexokinase 2 by sponging microrna-484 to promote the malignancy of colorectal cancer
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7700093/
https://www.ncbi.nlm.nih.gov/pubmed/33262654
http://dx.doi.org/10.2147/CMAR.S262096
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