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NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1
BACKGROUND: Stomach adenocarcinoma (STAD) is the most common type of gastric cancer (GC), with a high recurrence rate and poor prognosis, but the potential indicators for STAD are insufficient. METHODS: Herein, we found that MicroRNA-378c (miR-378c) was lowly expressed in STAD, and the low expressio...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8842946/ https://www.ncbi.nlm.nih.gov/pubmed/35164743 http://dx.doi.org/10.1186/s12935-022-02474-5 |
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author | Hu, Yongjun Luo, Ming |
author_facet | Hu, Yongjun Luo, Ming |
author_sort | Hu, Yongjun |
collection | PubMed |
description | BACKGROUND: Stomach adenocarcinoma (STAD) is the most common type of gastric cancer (GC), with a high recurrence rate and poor prognosis, but the potential indicators for STAD are insufficient. METHODS: Herein, we found that MicroRNA-378c (miR-378c) was lowly expressed in STAD, and the low expression of miR-378c was highly correlated with poor overall survival (OS), T stage, Reflux history, DSS events and PFI events of STAD patients. RESULTS: In addition, univariate analysis displayed that miR-378c was significantly associated with OS (Hazard ratio 0.735; 95% CI, 0.542–0.995; P = 0.046). Furthermore, it was validated that miR-378c inhibition accelerated STAD cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), while they were suppressed by miR-378c overexpression. Mechanistically, Neuropilin 1 (NRP1) was confirmed as the target of miR-378c, and Lnc-NORAD was identified as its sponger. More importantly, NORAD-mediated miR-378c inhibited malignant behaviors of STAD both in vitro and in vivo. CONCLUSIONS: Collectively, these results suggest miR-378c as a promising indicator for the treatment of STAD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12935-022-02474-5. |
format | Online Article Text |
id | pubmed-8842946 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-88429462022-02-16 NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1 Hu, Yongjun Luo, Ming Cancer Cell Int Primary Research BACKGROUND: Stomach adenocarcinoma (STAD) is the most common type of gastric cancer (GC), with a high recurrence rate and poor prognosis, but the potential indicators for STAD are insufficient. METHODS: Herein, we found that MicroRNA-378c (miR-378c) was lowly expressed in STAD, and the low expression of miR-378c was highly correlated with poor overall survival (OS), T stage, Reflux history, DSS events and PFI events of STAD patients. RESULTS: In addition, univariate analysis displayed that miR-378c was significantly associated with OS (Hazard ratio 0.735; 95% CI, 0.542–0.995; P = 0.046). Furthermore, it was validated that miR-378c inhibition accelerated STAD cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), while they were suppressed by miR-378c overexpression. Mechanistically, Neuropilin 1 (NRP1) was confirmed as the target of miR-378c, and Lnc-NORAD was identified as its sponger. More importantly, NORAD-mediated miR-378c inhibited malignant behaviors of STAD both in vitro and in vivo. CONCLUSIONS: Collectively, these results suggest miR-378c as a promising indicator for the treatment of STAD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12935-022-02474-5. BioMed Central 2022-02-14 /pmc/articles/PMC8842946/ /pubmed/35164743 http://dx.doi.org/10.1186/s12935-022-02474-5 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Primary Research Hu, Yongjun Luo, Ming NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1 |
title | NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1 |
title_full | NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1 |
title_fullStr | NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1 |
title_full_unstemmed | NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1 |
title_short | NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1 |
title_sort | norad-sponged mir-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting nrp1 |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8842946/ https://www.ncbi.nlm.nih.gov/pubmed/35164743 http://dx.doi.org/10.1186/s12935-022-02474-5 |
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