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LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis

Chordoma is a malignant bone tumor originating from the embryonic remnants of the notochord. lncRNAs act as competing endogenous RNAs (ceRNAs) and play a critical role in tumor pathology. However, the biological role of lncRNA-NONHSAT024778 and the underlying molecular mechanism in chordoma remains...

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Autores principales: Wang, Bin, Zhang, Kai, Meng, Sen, Shao, Xiaofeng, Zhou, Zhangzhe, Mao, Haiqing, Zhu, Ziqiang, Chen, Hao, Yang, Huilin, Chen, Kangwu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7975704/
https://www.ncbi.nlm.nih.gov/pubmed/33767589
http://dx.doi.org/10.7150/ijbs.54091
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author Wang, Bin
Zhang, Kai
Meng, Sen
Shao, Xiaofeng
Zhou, Zhangzhe
Mao, Haiqing
Zhu, Ziqiang
Chen, Hao
Yang, Huilin
Chen, Kangwu
author_facet Wang, Bin
Zhang, Kai
Meng, Sen
Shao, Xiaofeng
Zhou, Zhangzhe
Mao, Haiqing
Zhu, Ziqiang
Chen, Hao
Yang, Huilin
Chen, Kangwu
author_sort Wang, Bin
collection PubMed
description Chordoma is a malignant bone tumor originating from the embryonic remnants of the notochord. lncRNAs act as competing endogenous RNAs (ceRNAs) and play a critical role in tumor pathology. However, the biological role of lncRNA-NONHSAT024778 and the underlying molecular mechanism in chordoma remains unknown. qRT-PCR was used to analyze the expression changes of NONHSAT024778 and miR-1290 in chordoma tissues and cell lines. Bioinformatics analysis and luciferase reporter assay were applied to detect the targeting binding effect between NONHSAT024778 and miR-1290, and between Robo1 and miR-1290. The effect of NONHSAT024778 on chordoma cell proliferation and invasion and its regulation of miR-1290 by acting as a ceRNA were also investigated. An increased NONHSAT024778 expression was correlated with a decreased miR-1290 level in chordoma tissues. NONHSAT024778 knockdown suppressed the proliferation and invasion of chordoma cells. miR-1290 restored expression rescued the carcinogenic function of NONHSAT024778. Bioinformatics analysis showed that NONHSAT024778 acted as ceRNA to regulate Robo1 via sponging miR-1290 in chordoma cells, thereby promoting chordoma cell malignant progression. In vivo results confirmed the anti-tumor effects of NONHSAT024778 knockdown activating miR-1290 to inhibit the oncogene Robo1. NONHSAT024778 is substantially overexpressed, whereas miR-1290 is decreased in chordoma tissue. NONHSAT024778-miR-1290-Robo1 axis plays a critical role in chordoma tumorigenesis and might be a potential predictive biomarker for the diagnosis and therapeutic target among patients with chordoma.
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spelling pubmed-79757042021-03-24 LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis Wang, Bin Zhang, Kai Meng, Sen Shao, Xiaofeng Zhou, Zhangzhe Mao, Haiqing Zhu, Ziqiang Chen, Hao Yang, Huilin Chen, Kangwu Int J Biol Sci Research Paper Chordoma is a malignant bone tumor originating from the embryonic remnants of the notochord. lncRNAs act as competing endogenous RNAs (ceRNAs) and play a critical role in tumor pathology. However, the biological role of lncRNA-NONHSAT024778 and the underlying molecular mechanism in chordoma remains unknown. qRT-PCR was used to analyze the expression changes of NONHSAT024778 and miR-1290 in chordoma tissues and cell lines. Bioinformatics analysis and luciferase reporter assay were applied to detect the targeting binding effect between NONHSAT024778 and miR-1290, and between Robo1 and miR-1290. The effect of NONHSAT024778 on chordoma cell proliferation and invasion and its regulation of miR-1290 by acting as a ceRNA were also investigated. An increased NONHSAT024778 expression was correlated with a decreased miR-1290 level in chordoma tissues. NONHSAT024778 knockdown suppressed the proliferation and invasion of chordoma cells. miR-1290 restored expression rescued the carcinogenic function of NONHSAT024778. Bioinformatics analysis showed that NONHSAT024778 acted as ceRNA to regulate Robo1 via sponging miR-1290 in chordoma cells, thereby promoting chordoma cell malignant progression. In vivo results confirmed the anti-tumor effects of NONHSAT024778 knockdown activating miR-1290 to inhibit the oncogene Robo1. NONHSAT024778 is substantially overexpressed, whereas miR-1290 is decreased in chordoma tissue. NONHSAT024778-miR-1290-Robo1 axis plays a critical role in chordoma tumorigenesis and might be a potential predictive biomarker for the diagnosis and therapeutic target among patients with chordoma. Ivyspring International Publisher 2021-02-08 /pmc/articles/PMC7975704/ /pubmed/33767589 http://dx.doi.org/10.7150/ijbs.54091 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Wang, Bin
Zhang, Kai
Meng, Sen
Shao, Xiaofeng
Zhou, Zhangzhe
Mao, Haiqing
Zhu, Ziqiang
Chen, Hao
Yang, Huilin
Chen, Kangwu
LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis
title LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis
title_full LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis
title_fullStr LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis
title_full_unstemmed LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis
title_short LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis
title_sort lncrna-nonhsat024778 promote the proliferation and invasion of chordoma cell by regulating mir-1290/robo1 axis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7975704/
https://www.ncbi.nlm.nih.gov/pubmed/33767589
http://dx.doi.org/10.7150/ijbs.54091
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