Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154

Renal carcinoma (RCC) is widely accepted as a malignant tumour of urinary system. Long intergenic non-coding RNA 1939 (LINC01939) is a novel lncRNA which was found to be down-regulated in RCC. Thus, we set out to explore the effect and regulation mechanism of LINC01939 in RCC. LINC01939 and miR-154...

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Main Authors: Rongyuan Zhang, Weijie Zhang, Baocai Xu, Chuan Lv, Jianquan Hou, Guangbo Zhang
Format: Article
Language:English
Published: Taylor & Francis Group 2020-01-01
Series:Artificial Cells, Nanomedicine, and Biotechnology
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Online Access:https://www.tandfonline.com/doi/10.1080/21691401.2020.1725024
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author Rongyuan Zhang
Weijie Zhang
Baocai Xu
Chuan Lv
Jianquan Hou
Guangbo Zhang
author_facet Rongyuan Zhang
Weijie Zhang
Baocai Xu
Chuan Lv
Jianquan Hou
Guangbo Zhang
author_sort Rongyuan Zhang
collection DOAJ
description Renal carcinoma (RCC) is widely accepted as a malignant tumour of urinary system. Long intergenic non-coding RNA 1939 (LINC01939) is a novel lncRNA which was found to be down-regulated in RCC. Thus, we set out to explore the effect and regulation mechanism of LINC01939 in RCC. LINC01939 and miR-154 in RCC tissues and cell lines were detected using qRT-PCR assay. To examine cellular viability of ACHN and CAKI-1 cells, cell counting kit-8 (CCK-8) assay was exploited here. Flow cytometric analysis was conducted to examine apoptosis. Cell mobility was valued through wound healing assays. Western blotting was applied for examination of proteins related to proliferation, apoptosis, migration and Wnt/β-catenin/Notch. LINC01939 was down-regulated in RCC tissues. LINC01939 overexpression impeded proliferation and migration, and induced apoptosis. Further study found that the overexpression of LINC01939 strongly suppressed miR-154 expression. Then, the inhibiting effect of overexpressed LINC01939 on proliferation and mobility and the promoting role of LINC01939 in apoptosis were abolished by the combination of miR-154 mimic. Finally, we found that overexpressed LINC01939 inactivated Wnt/β-catenin and Notch through suppressing miR-154. Up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.
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spelling doaj-art-fb2932ee2c9646a4a7e1d2a19b95cede2025-08-20T04:02:41ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2020-01-0148169570210.1080/21691401.2020.1725024Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154Rongyuan Zhang0Weijie Zhang1Baocai Xu2Chuan Lv3Jianquan Hou4Guangbo Zhang5Department of Urology, The First Affiliated Hospital of Soochow University, Jiangsu, ChinaDepartment of Urology, The First Affiliated Hospital of Soochow University, Jiangsu, ChinaDepartment of Urology, Jining No, 1 People’s Hospital, Jining, ChinaDepartment of Urology, Jining No, 1 People’s Hospital, Jining, ChinaDepartment of Urology, The First Affiliated Hospital of Soochow University, Jiangsu, ChinaJiangsu Institute of Clinical Immunology, The First Affiliated Hospital of Soochow University, Jiangsu, ChinaRenal carcinoma (RCC) is widely accepted as a malignant tumour of urinary system. Long intergenic non-coding RNA 1939 (LINC01939) is a novel lncRNA which was found to be down-regulated in RCC. Thus, we set out to explore the effect and regulation mechanism of LINC01939 in RCC. LINC01939 and miR-154 in RCC tissues and cell lines were detected using qRT-PCR assay. To examine cellular viability of ACHN and CAKI-1 cells, cell counting kit-8 (CCK-8) assay was exploited here. Flow cytometric analysis was conducted to examine apoptosis. Cell mobility was valued through wound healing assays. Western blotting was applied for examination of proteins related to proliferation, apoptosis, migration and Wnt/β-catenin/Notch. LINC01939 was down-regulated in RCC tissues. LINC01939 overexpression impeded proliferation and migration, and induced apoptosis. Further study found that the overexpression of LINC01939 strongly suppressed miR-154 expression. Then, the inhibiting effect of overexpressed LINC01939 on proliferation and mobility and the promoting role of LINC01939 in apoptosis were abolished by the combination of miR-154 mimic. Finally, we found that overexpressed LINC01939 inactivated Wnt/β-catenin and Notch through suppressing miR-154. Up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.https://www.tandfonline.com/doi/10.1080/21691401.2020.1725024Renal carcinomaLINC01939miR-154proliferationmigration
spellingShingle Rongyuan Zhang
Weijie Zhang
Baocai Xu
Chuan Lv
Jianquan Hou
Guangbo Zhang
Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154
Artificial Cells, Nanomedicine, and Biotechnology
Renal carcinoma
LINC01939
miR-154
proliferation
migration
title Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154
title_full Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154
title_fullStr Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154
title_full_unstemmed Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154
title_short Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154
title_sort long intergenic non coding rna 1939 eliminates proliferation and migration of human renal cell carcinoma rcc cells by down regulation of mir 154
topic Renal carcinoma
LINC01939
miR-154
proliferation
migration
url https://www.tandfonline.com/doi/10.1080/21691401.2020.1725024
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