Long non-coding RNA LINC01559 serves as a competing endogenous RNA accelerating triple-negative breast cancer progression

Background: Long non-coding RNA (lncRNA) is an endogenous RNA over 200 nt in length involved in gene regulation. LINC01559 is a novel lncRNA that has been identified as a fundamental player in human cancer. However, its role in triple-negative breast cancer (TNBC) remains unknown. Here, we explored...

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Main Authors: Xue Yang, Yunqing Yang, Xueke Qian, Xiaodong Xu, Pengwei Lv
Format: Article
Language:English
Published: Elsevier 2022-06-01
Series:Biomedical Journal
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2319417021000597
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author Xue Yang
Yunqing Yang
Xueke Qian
Xiaodong Xu
Pengwei Lv
author_facet Xue Yang
Yunqing Yang
Xueke Qian
Xiaodong Xu
Pengwei Lv
author_sort Xue Yang
collection DOAJ
description Background: Long non-coding RNA (lncRNA) is an endogenous RNA over 200 nt in length involved in gene regulation. LINC01559 is a novel lncRNA that has been identified as a fundamental player in human cancer. However, its role in triple-negative breast cancer (TNBC) remains unknown. Here, we explored the expression, function and clinical implication of LINC01559 in TNBC. Methods: RNA expression was detected by qRT-PCR analysis. Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU), wound healing and Transwell assays were used to test cell viability, DNA synthesis rate, migration and invasion, respectively. The competing endogenous RNA (ceRNA) axis involved in LINC01559 was determined by RNA pull-down and luciferase reporter assays. The xenograft model was used to verify the function of LINC01559 in vivo. Results: LINC01559 was significantly increased in TNBC tissues as compared to matched normal tissues, which was due to high levels of H3K4Me3 and H3K27Ac in the promoter region. Knockdown of LINC01559 inhibited TNBC cell proliferation, migration and invasion in vitro, and also retarded tumor growth and reduced lung metastasis in vivo. Mechanistically, LINC01559 served as a ceRNA that sponged miR-370-3p, miR-485-5p and miR-940, resulting in increasing the expression of a cohort of oncogenes, thus accelerating TNBC progression. Conclusions: Our data provide a comprehensive analysis of LINC01559 in TNBC, we found that LINC01559 functioned as a carcinogenic ceRNA via sponging miRNAs. Targeting of LINC01559 may be a potential treatment for TNBC patients.
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spelling doaj.art-2a327304fe3544a0bd11ed2a82c3afa42022-12-22T04:02:00ZengElsevierBiomedical Journal2319-41702022-06-01453512521Long non-coding RNA LINC01559 serves as a competing endogenous RNA accelerating triple-negative breast cancer progressionXue Yang0Yunqing Yang1Xueke Qian2Xiaodong Xu3Pengwei Lv4Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Henan, ChinaBreast Surgery, The First Affiliated Hospital of Zhengzhou University, Henan, ChinaBreast Surgery, The First Affiliated Hospital of Zhengzhou University, Henan, ChinaBreast Surgery, The First Affiliated Hospital of Zhengzhou University, Henan, ChinaCorresponding author. Breast Surgery, The First Affiliated Hospital of Zhengzhou University, 1, Jianshe E Rd, Erqi, Zhengzhou 45000, Henan, China.; Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Henan, ChinaBackground: Long non-coding RNA (lncRNA) is an endogenous RNA over 200 nt in length involved in gene regulation. LINC01559 is a novel lncRNA that has been identified as a fundamental player in human cancer. However, its role in triple-negative breast cancer (TNBC) remains unknown. Here, we explored the expression, function and clinical implication of LINC01559 in TNBC. Methods: RNA expression was detected by qRT-PCR analysis. Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU), wound healing and Transwell assays were used to test cell viability, DNA synthesis rate, migration and invasion, respectively. The competing endogenous RNA (ceRNA) axis involved in LINC01559 was determined by RNA pull-down and luciferase reporter assays. The xenograft model was used to verify the function of LINC01559 in vivo. Results: LINC01559 was significantly increased in TNBC tissues as compared to matched normal tissues, which was due to high levels of H3K4Me3 and H3K27Ac in the promoter region. Knockdown of LINC01559 inhibited TNBC cell proliferation, migration and invasion in vitro, and also retarded tumor growth and reduced lung metastasis in vivo. Mechanistically, LINC01559 served as a ceRNA that sponged miR-370-3p, miR-485-5p and miR-940, resulting in increasing the expression of a cohort of oncogenes, thus accelerating TNBC progression. Conclusions: Our data provide a comprehensive analysis of LINC01559 in TNBC, we found that LINC01559 functioned as a carcinogenic ceRNA via sponging miRNAs. Targeting of LINC01559 may be a potential treatment for TNBC patients.http://www.sciencedirect.com/science/article/pii/S2319417021000597LncRNALINC01559ceRNATNBCHistone modification
spellingShingle Xue Yang
Yunqing Yang
Xueke Qian
Xiaodong Xu
Pengwei Lv
Long non-coding RNA LINC01559 serves as a competing endogenous RNA accelerating triple-negative breast cancer progression
Biomedical Journal
LncRNA
LINC01559
ceRNA
TNBC
Histone modification
title Long non-coding RNA LINC01559 serves as a competing endogenous RNA accelerating triple-negative breast cancer progression
title_full Long non-coding RNA LINC01559 serves as a competing endogenous RNA accelerating triple-negative breast cancer progression
title_fullStr Long non-coding RNA LINC01559 serves as a competing endogenous RNA accelerating triple-negative breast cancer progression
title_full_unstemmed Long non-coding RNA LINC01559 serves as a competing endogenous RNA accelerating triple-negative breast cancer progression
title_short Long non-coding RNA LINC01559 serves as a competing endogenous RNA accelerating triple-negative breast cancer progression
title_sort long non coding rna linc01559 serves as a competing endogenous rna accelerating triple negative breast cancer progression
topic LncRNA
LINC01559
ceRNA
TNBC
Histone modification
url http://www.sciencedirect.com/science/article/pii/S2319417021000597
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