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LINC01128 facilitates the progression of pancreatic cancer through up-regulation of LDHA by targeting miR-561-5p
BACKGROUND: Long non-coding RNAs (lncRNAs) regulate tumor development and metastasis in several types of cancers through various molecular mechanisms. However, the biological role of most lncRNAs in pancreatic cancer (PC) remains unclear. Here, we explored the expression, biological functions, and m...
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/PMC8862213/ https://www.ncbi.nlm.nih.gov/pubmed/35193567 http://dx.doi.org/10.1186/s12935-022-02490-5 |
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author | Zhong, Min Fang, Zhi Ruan, Bin Xiong, Jianping Li, Junhe Song, Zhiwang |
author_facet | Zhong, Min Fang, Zhi Ruan, Bin Xiong, Jianping Li, Junhe Song, Zhiwang |
author_sort | Zhong, Min |
collection | PubMed |
description | BACKGROUND: Long non-coding RNAs (lncRNAs) regulate tumor development and metastasis in several types of cancers through various molecular mechanisms. However, the biological role of most lncRNAs in pancreatic cancer (PC) remains unclear. Here, we explored the expression, biological functions, and molecular mechanism of LINC01128 in PC. METHODS: Quantitive reverse transcription PCR was used to detect the expression level of LINC01128 in PC tissues and different PC cell lines. A loss-of-function and gain-of-function experiment was used to explore the biological effects of LINC01128 on PC carcinogenesis in vitro and in vivo. Western blot analysis, subcellular fractionation experiment, luciferase reporter gene assay, and MS2-RNA immunoprecipitation experiment were used to study the potential molecular mechanism of LINC01128 during carcinogenesis. RESULTS: The expression of LINC01128 was upregulated in PC tissues and cell lines, and overexpression of LINC01128 was significantly related to the poor prognosis of patients with PC. Furthermore, silencing LINC01128 significantly inhibited the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of PC cells in vitro and tumor growth in vivo, while LINC01128 overexpression promoted these processes. Further research showed that LINC01128 acted as a sponge for microRNA miR-561-5p, and lactate dehydrogenase A (LDHA) was the downstream target gene of miR-561-5p. It was also revealed that the expression of miR-561-5p in PC was decreased, and a negative correlation between miR-561-5p and LINC01128 was revealed. Based on rescue experiments, LDHA overexpression partially restored the inhibitory effect of LINC01128 knockdown on proliferation, migration, and invasion of PC cells. CONCLUSIONS: LINC01128 promotes the proliferation, migration, invasion, and EMT of PC by regulating the miR-561-5p/LDHA axis, suggesting LINC01128 may be a new prognostic marker and therapeutic target in PC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12935-022-02490-5. |
format | Online Article Text |
id | pubmed-8862213 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-88622132022-02-23 LINC01128 facilitates the progression of pancreatic cancer through up-regulation of LDHA by targeting miR-561-5p Zhong, Min Fang, Zhi Ruan, Bin Xiong, Jianping Li, Junhe Song, Zhiwang Cancer Cell Int Primary Research BACKGROUND: Long non-coding RNAs (lncRNAs) regulate tumor development and metastasis in several types of cancers through various molecular mechanisms. However, the biological role of most lncRNAs in pancreatic cancer (PC) remains unclear. Here, we explored the expression, biological functions, and molecular mechanism of LINC01128 in PC. METHODS: Quantitive reverse transcription PCR was used to detect the expression level of LINC01128 in PC tissues and different PC cell lines. A loss-of-function and gain-of-function experiment was used to explore the biological effects of LINC01128 on PC carcinogenesis in vitro and in vivo. Western blot analysis, subcellular fractionation experiment, luciferase reporter gene assay, and MS2-RNA immunoprecipitation experiment were used to study the potential molecular mechanism of LINC01128 during carcinogenesis. RESULTS: The expression of LINC01128 was upregulated in PC tissues and cell lines, and overexpression of LINC01128 was significantly related to the poor prognosis of patients with PC. Furthermore, silencing LINC01128 significantly inhibited the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of PC cells in vitro and tumor growth in vivo, while LINC01128 overexpression promoted these processes. Further research showed that LINC01128 acted as a sponge for microRNA miR-561-5p, and lactate dehydrogenase A (LDHA) was the downstream target gene of miR-561-5p. It was also revealed that the expression of miR-561-5p in PC was decreased, and a negative correlation between miR-561-5p and LINC01128 was revealed. Based on rescue experiments, LDHA overexpression partially restored the inhibitory effect of LINC01128 knockdown on proliferation, migration, and invasion of PC cells. CONCLUSIONS: LINC01128 promotes the proliferation, migration, invasion, and EMT of PC by regulating the miR-561-5p/LDHA axis, suggesting LINC01128 may be a new prognostic marker and therapeutic target in PC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12935-022-02490-5. BioMed Central 2022-02-22 /pmc/articles/PMC8862213/ /pubmed/35193567 http://dx.doi.org/10.1186/s12935-022-02490-5 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 Zhong, Min Fang, Zhi Ruan, Bin Xiong, Jianping Li, Junhe Song, Zhiwang LINC01128 facilitates the progression of pancreatic cancer through up-regulation of LDHA by targeting miR-561-5p |
title | LINC01128 facilitates the progression of pancreatic cancer through up-regulation of LDHA by targeting miR-561-5p |
title_full | LINC01128 facilitates the progression of pancreatic cancer through up-regulation of LDHA by targeting miR-561-5p |
title_fullStr | LINC01128 facilitates the progression of pancreatic cancer through up-regulation of LDHA by targeting miR-561-5p |
title_full_unstemmed | LINC01128 facilitates the progression of pancreatic cancer through up-regulation of LDHA by targeting miR-561-5p |
title_short | LINC01128 facilitates the progression of pancreatic cancer through up-regulation of LDHA by targeting miR-561-5p |
title_sort | linc01128 facilitates the progression of pancreatic cancer through up-regulation of ldha by targeting mir-561-5p |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8862213/ https://www.ncbi.nlm.nih.gov/pubmed/35193567 http://dx.doi.org/10.1186/s12935-022-02490-5 |
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