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KIAA1522 Promotes the Progression of Hepatocellular Carcinoma via the Activation of the Wnt/β-Catenin Signaling Pathway

PURPOSE: KIAA1522 was previously identified to play a crucial role in cancer development and progression. However, its functions and underlying mechanisms in hepatocellular carcinoma (HCC) remain elusive. MATERIALS AND METHODS: To elucidate the role of KIAA1522 in HCC, its expression was assessed us...

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Autores principales: Jiang, Shunbin, Zhang, Yonggang, Li, Qing, Qiu, Lei, Bian, Baoxiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305824/
https://www.ncbi.nlm.nih.gov/pubmed/32606779
http://dx.doi.org/10.2147/OTT.S251157
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author Jiang, Shunbin
Zhang, Yonggang
Li, Qing
Qiu, Lei
Bian, Baoxiang
author_facet Jiang, Shunbin
Zhang, Yonggang
Li, Qing
Qiu, Lei
Bian, Baoxiang
author_sort Jiang, Shunbin
collection PubMed
description PURPOSE: KIAA1522 was previously identified to play a crucial role in cancer development and progression. However, its functions and underlying mechanisms in hepatocellular carcinoma (HCC) remain elusive. MATERIALS AND METHODS: To elucidate the role of KIAA1522 in HCC, its expression was assessed using The Cancer Genome Atlas and GEPIA databases. Next, these results were validated by quantitative reverse transcription-polymerase chain reaction, Western blotting, and immunohistochemistry of HCC tissues and cell lines. Flow cytometry, CCK-8, EDU, colony formation, Transwell invasion, and wound healing assays were performed to explore the function of KIAA1522 in HCC in vivo and in vitro. Finally, gene set enrichment analysis was used to identify the pathways involved. RESULTS: Our results demonstrated that KIAA1522 was highly expressed in HCC tissues and cell lines. Furthermore, KIAA1522 overexpression was associated with unfavorable clinicopathological characteristics. Survival analyses revealed that KIAA1522 overexpression predicted lower recurrence-free and overall survival rates in patients with HCC. Functional studies suggested that KIAA1522 facilitated HCC proliferation, migration, and invasion both in vitro and in vivo. Moreover, KIAA1522 up-regulated the Wnt/β-catenin signaling pathway, as confirmed by TOP-flash/FOP-flash luciferase reporter assays and Western blotting. CONCLUSION: In conclusion, we highlighted the oncogenic role of KIAA1522 in HCC and determined its potential as a therapeutic target for HCC.
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spelling pubmed-73058242020-06-29 KIAA1522 Promotes the Progression of Hepatocellular Carcinoma via the Activation of the Wnt/β-Catenin Signaling Pathway Jiang, Shunbin Zhang, Yonggang Li, Qing Qiu, Lei Bian, Baoxiang Onco Targets Ther Original Research PURPOSE: KIAA1522 was previously identified to play a crucial role in cancer development and progression. However, its functions and underlying mechanisms in hepatocellular carcinoma (HCC) remain elusive. MATERIALS AND METHODS: To elucidate the role of KIAA1522 in HCC, its expression was assessed using The Cancer Genome Atlas and GEPIA databases. Next, these results were validated by quantitative reverse transcription-polymerase chain reaction, Western blotting, and immunohistochemistry of HCC tissues and cell lines. Flow cytometry, CCK-8, EDU, colony formation, Transwell invasion, and wound healing assays were performed to explore the function of KIAA1522 in HCC in vivo and in vitro. Finally, gene set enrichment analysis was used to identify the pathways involved. RESULTS: Our results demonstrated that KIAA1522 was highly expressed in HCC tissues and cell lines. Furthermore, KIAA1522 overexpression was associated with unfavorable clinicopathological characteristics. Survival analyses revealed that KIAA1522 overexpression predicted lower recurrence-free and overall survival rates in patients with HCC. Functional studies suggested that KIAA1522 facilitated HCC proliferation, migration, and invasion both in vitro and in vivo. Moreover, KIAA1522 up-regulated the Wnt/β-catenin signaling pathway, as confirmed by TOP-flash/FOP-flash luciferase reporter assays and Western blotting. CONCLUSION: In conclusion, we highlighted the oncogenic role of KIAA1522 in HCC and determined its potential as a therapeutic target for HCC. Dove 2020-06-16 /pmc/articles/PMC7305824/ /pubmed/32606779 http://dx.doi.org/10.2147/OTT.S251157 Text en © 2020 Jiang 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
Jiang, Shunbin
Zhang, Yonggang
Li, Qing
Qiu, Lei
Bian, Baoxiang
KIAA1522 Promotes the Progression of Hepatocellular Carcinoma via the Activation of the Wnt/β-Catenin Signaling Pathway
title KIAA1522 Promotes the Progression of Hepatocellular Carcinoma via the Activation of the Wnt/β-Catenin Signaling Pathway
title_full KIAA1522 Promotes the Progression of Hepatocellular Carcinoma via the Activation of the Wnt/β-Catenin Signaling Pathway
title_fullStr KIAA1522 Promotes the Progression of Hepatocellular Carcinoma via the Activation of the Wnt/β-Catenin Signaling Pathway
title_full_unstemmed KIAA1522 Promotes the Progression of Hepatocellular Carcinoma via the Activation of the Wnt/β-Catenin Signaling Pathway
title_short KIAA1522 Promotes the Progression of Hepatocellular Carcinoma via the Activation of the Wnt/β-Catenin Signaling Pathway
title_sort kiaa1522 promotes the progression of hepatocellular carcinoma via the activation of the wnt/β-catenin signaling pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305824/
https://www.ncbi.nlm.nih.gov/pubmed/32606779
http://dx.doi.org/10.2147/OTT.S251157
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