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Knockdown of lncRNA HAGLROS inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy
Nephroblastoma, or Wilms tumor, is a primary renal malignant tumor that easily occurs in children. Previous studies have revealed the regulatory functions of LncRNA in nephroblastoma. LncRNA HAGLROS functions as a tumor promotor in various cancers including hepatocellular carcinoma, ovarian cancer a...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9208483/ https://www.ncbi.nlm.nih.gov/pubmed/35358010 http://dx.doi.org/10.1080/21655979.2021.2023984 |
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author | Li, Pugui Zhang, Kun Tang, Shijie Tang, Weizhu |
author_facet | Li, Pugui Zhang, Kun Tang, Shijie Tang, Weizhu |
author_sort | Li, Pugui |
collection | PubMed |
description | Nephroblastoma, or Wilms tumor, is a primary renal malignant tumor that easily occurs in children. Previous studies have revealed the regulatory functions of LncRNA in nephroblastoma. LncRNA HAGLROS functions as a tumor promotor in various cancers including hepatocellular carcinoma, ovarian cancer and colorectal cancer. In this study, the HAGLROS expression in nephroblastoma cells was assayed through qRT-PCR. Cell proliferation assessment employed CCK-8. Moreover, the migration and invasion of cells were examined separately through wound healing and transwell assay. Moreover, flow cytometric analysis and Western blot assay were applied to evaluate cell apoptosis. Rapamycin and 3-methyladenine were used to serve as autophagy activator or inhibitor, respectively. In addition, autophagy was identified by immunofluorescence staining and Western blot analysis. Experiment results showed that HAGLROS expressed highly in nephroblastoma cell lines. HAGLROS knockdown prevented cells from proliferating, and also showed suppressive impact on migration and invasion in HFWT cells. In addition, knockdown of HAGLROS showed a facilitative effect on apoptosis and an inhibitory effect on autophagy. Stimulation of autophagy alleviated HAGLROS silencing-induced apoptosis, while inhibition of autophagy reversed the effect in nephroblastoma cells. In summary, our results revealed that HAGLROS executed an oncogenic role in the progress of nephroblastoma, offering a new perspective on the strategy for nephroblastoma therapy. |
format | Online Article Text |
id | pubmed-9208483 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-92084832022-06-21 Knockdown of lncRNA HAGLROS inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy Li, Pugui Zhang, Kun Tang, Shijie Tang, Weizhu Bioengineered Research Paper Nephroblastoma, or Wilms tumor, is a primary renal malignant tumor that easily occurs in children. Previous studies have revealed the regulatory functions of LncRNA in nephroblastoma. LncRNA HAGLROS functions as a tumor promotor in various cancers including hepatocellular carcinoma, ovarian cancer and colorectal cancer. In this study, the HAGLROS expression in nephroblastoma cells was assayed through qRT-PCR. Cell proliferation assessment employed CCK-8. Moreover, the migration and invasion of cells were examined separately through wound healing and transwell assay. Moreover, flow cytometric analysis and Western blot assay were applied to evaluate cell apoptosis. Rapamycin and 3-methyladenine were used to serve as autophagy activator or inhibitor, respectively. In addition, autophagy was identified by immunofluorescence staining and Western blot analysis. Experiment results showed that HAGLROS expressed highly in nephroblastoma cell lines. HAGLROS knockdown prevented cells from proliferating, and also showed suppressive impact on migration and invasion in HFWT cells. In addition, knockdown of HAGLROS showed a facilitative effect on apoptosis and an inhibitory effect on autophagy. Stimulation of autophagy alleviated HAGLROS silencing-induced apoptosis, while inhibition of autophagy reversed the effect in nephroblastoma cells. In summary, our results revealed that HAGLROS executed an oncogenic role in the progress of nephroblastoma, offering a new perspective on the strategy for nephroblastoma therapy. Taylor & Francis 2022-03-31 /pmc/articles/PMC9208483/ /pubmed/35358010 http://dx.doi.org/10.1080/21655979.2021.2023984 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Li, Pugui Zhang, Kun Tang, Shijie Tang, Weizhu Knockdown of lncRNA HAGLROS inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy |
title | Knockdown of lncRNA HAGLROS inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy |
title_full | Knockdown of lncRNA HAGLROS inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy |
title_fullStr | Knockdown of lncRNA HAGLROS inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy |
title_full_unstemmed | Knockdown of lncRNA HAGLROS inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy |
title_short | Knockdown of lncRNA HAGLROS inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy |
title_sort | knockdown of lncrna haglros inhibits metastasis and promotes apoptosis in nephroblastoma cells by inhibition of autophagy |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9208483/ https://www.ncbi.nlm.nih.gov/pubmed/35358010 http://dx.doi.org/10.1080/21655979.2021.2023984 |
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