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Circ-SNX27 sponging miR-375/RPN1 axis contributes to hepatocellular carcinoma progression

Hepatocellular carcinoma (HCC) is a prevalent malignant tumor with high fatality. It has yet to be reported whether circ-SNX27 can affect the progression of HCC. This study attempted to analyze circ-SNX27’s precise role and underlying mechanisms in HCC. HCC cell lines and tumor specimens from HCC pa...

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Autores principales: Zheng, Chao, Liang, Jin, Yu, Shoude, Xu, Hua, Dai, Lin, Xu, Dan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Physiological Society and The Korean Society of Pharmacology 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10316188/
https://www.ncbi.nlm.nih.gov/pubmed/37386831
http://dx.doi.org/10.4196/kjpp.2023.27.4.333
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author Zheng, Chao
Liang, Jin
Yu, Shoude
Xu, Hua
Dai, Lin
Xu, Dan
author_facet Zheng, Chao
Liang, Jin
Yu, Shoude
Xu, Hua
Dai, Lin
Xu, Dan
author_sort Zheng, Chao
collection PubMed
description Hepatocellular carcinoma (HCC) is a prevalent malignant tumor with high fatality. It has yet to be reported whether circ-SNX27 can affect the progression of HCC. This study attempted to analyze circ-SNX27’s precise role and underlying mechanisms in HCC. HCC cell lines and tumor specimens from HCC patients were analyzed using quantitative real-time PCR and Western blotting to quantify the expressions of circ-SNX27, miR-375, and ribophorin I (RPN1). Cell invasion and cell counting kit 8 experiments were conducted for the evaluation of HCC cell invasion and proliferation. Caspase-3 Activity Assay Kit was utilized to gauge the caspase-3 activity. Luciferase reporter and RNA immunoprecipitation assays were executed to ascertain the relationships among miR-375, circ-SNX27, and RPN1. To determine how circ-SNX27 knockdown affects the growth of HCC xenografts in vivo, tumor-bearing mouse models were constructed. Elevated expressions of circ-SNX27 and RPN1 as well as a reduced miR-375 expression were observed among HCC cells and HCC patient tumor specimens. Knocking-down circ-SNX27 in HCC cells abated their proliferative and invasive abilities but raised their caspase-3 activity. Moreover, the poor levels of circ-SNX27 inhibited HCC tumor growth among the mice. Circ-SNX27 enhanced RPN1 by competitively binding with miR-375. Silencing miR-375 in HCC cells promoted their malignant phenotypes. Nonetheless, the promotive effect of miR-375 silencing was reversible via the knockdown of circ-SNX27 or RPN1. This research demonstrated that circ-SNX27 accelerated the progression of HCC by modulating the miR-375/RPN1 axis. This is indicative of circ-SNX27’s potential as a target for the treatment of HCC.
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spelling pubmed-103161882023-07-04 Circ-SNX27 sponging miR-375/RPN1 axis contributes to hepatocellular carcinoma progression Zheng, Chao Liang, Jin Yu, Shoude Xu, Hua Dai, Lin Xu, Dan Korean J Physiol Pharmacol Original Article Hepatocellular carcinoma (HCC) is a prevalent malignant tumor with high fatality. It has yet to be reported whether circ-SNX27 can affect the progression of HCC. This study attempted to analyze circ-SNX27’s precise role and underlying mechanisms in HCC. HCC cell lines and tumor specimens from HCC patients were analyzed using quantitative real-time PCR and Western blotting to quantify the expressions of circ-SNX27, miR-375, and ribophorin I (RPN1). Cell invasion and cell counting kit 8 experiments were conducted for the evaluation of HCC cell invasion and proliferation. Caspase-3 Activity Assay Kit was utilized to gauge the caspase-3 activity. Luciferase reporter and RNA immunoprecipitation assays were executed to ascertain the relationships among miR-375, circ-SNX27, and RPN1. To determine how circ-SNX27 knockdown affects the growth of HCC xenografts in vivo, tumor-bearing mouse models were constructed. Elevated expressions of circ-SNX27 and RPN1 as well as a reduced miR-375 expression were observed among HCC cells and HCC patient tumor specimens. Knocking-down circ-SNX27 in HCC cells abated their proliferative and invasive abilities but raised their caspase-3 activity. Moreover, the poor levels of circ-SNX27 inhibited HCC tumor growth among the mice. Circ-SNX27 enhanced RPN1 by competitively binding with miR-375. Silencing miR-375 in HCC cells promoted their malignant phenotypes. Nonetheless, the promotive effect of miR-375 silencing was reversible via the knockdown of circ-SNX27 or RPN1. This research demonstrated that circ-SNX27 accelerated the progression of HCC by modulating the miR-375/RPN1 axis. This is indicative of circ-SNX27’s potential as a target for the treatment of HCC. The Korean Physiological Society and The Korean Society of Pharmacology 2023-07-01 2023-07-01 /pmc/articles/PMC10316188/ /pubmed/37386831 http://dx.doi.org/10.4196/kjpp.2023.27.4.333 Text en Copyright © Korean J Physiol Pharmacol https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0 (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Zheng, Chao
Liang, Jin
Yu, Shoude
Xu, Hua
Dai, Lin
Xu, Dan
Circ-SNX27 sponging miR-375/RPN1 axis contributes to hepatocellular carcinoma progression
title Circ-SNX27 sponging miR-375/RPN1 axis contributes to hepatocellular carcinoma progression
title_full Circ-SNX27 sponging miR-375/RPN1 axis contributes to hepatocellular carcinoma progression
title_fullStr Circ-SNX27 sponging miR-375/RPN1 axis contributes to hepatocellular carcinoma progression
title_full_unstemmed Circ-SNX27 sponging miR-375/RPN1 axis contributes to hepatocellular carcinoma progression
title_short Circ-SNX27 sponging miR-375/RPN1 axis contributes to hepatocellular carcinoma progression
title_sort circ-snx27 sponging mir-375/rpn1 axis contributes to hepatocellular carcinoma progression
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10316188/
https://www.ncbi.nlm.nih.gov/pubmed/37386831
http://dx.doi.org/10.4196/kjpp.2023.27.4.333
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