Long noncoding RNA TUG1 regulates prostate cancer cell proliferation, invasion and migration via the Nrf2 signaling axis

Long noncoding RNAs (lncRNAs) have been identified to modulate the development and progression of prostate cancer (PCa) via the regulation of their target genes. However, the biological function underlying the effect of lncRNA TUG1 in PCa remains unclear. Reverse transcription-quantitative polymeras...

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Veröffentlicht in:Pathology, research and practice research and practice, 2020-04, Vol.216 (4), p.152851-152851, Article 152851
Hauptverfasser: Yang, Guang, Yin, Hubin, Lin, Fan, Gao, Shun, Zhan, Kai, Tong, Hang, Tang, Xueyong, Pan, Qi, Gou, Xin
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container_issue 4
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container_title Pathology, research and practice
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creator Yang, Guang
Yin, Hubin
Lin, Fan
Gao, Shun
Zhan, Kai
Tong, Hang
Tang, Xueyong
Pan, Qi
Gou, Xin
description Long noncoding RNAs (lncRNAs) have been identified to modulate the development and progression of prostate cancer (PCa) via the regulation of their target genes. However, the biological function underlying the effect of lncRNA TUG1 in PCa remains unclear. Reverse transcription-quantitative polymerase chain reaction (qRT-PCR) and Western blotting analysis were used to assess the mRNA expression of TUG1 and protein expression levels of Nrf2 pathway members, respectively. The migration, invasion, and proliferation abilities of cells were assessed by the wound-healing, Transwell migration/invasion, and CCK8 assays, respectively. TUG1 was strikingly upregulated in PCa cells compared with non-tumorigenic human prostate epithelial cells. The LncTar Web Server, which is a bioinformatics tool, was used to predict the target association between TUG1 and Nrf2. Moreover, the expression of TUG1 showed a strikingly positive correlation with that of Nrf2 in TCGA PCa RNA-Seq data (r = 0.26,P = 4.63E-09). Subsequently, inhibition of TUG1 using siRNA resulted in deceased proliferation, migration, and invasion of PCa cells; however, these effects were reversed by treatment with oltipraz (an activator of Nrf2). Finally, we evaluated the Nrf2 pathway to reveal the underlying mechanism of TUG1 in PCa cells, and found that TUG1 knockdown decreased the protein expression of Nrf2 downstream members (e.g., HO-1, FTH1, and NQO1). LncRNA TUG1 plays an oncogenic role in human PCa cells by promoting the cell proliferation and invasion in PCa cell lines, at least partly via the Nrf2 signaling pathway.
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However, the biological function underlying the effect of lncRNA TUG1 in PCa remains unclear. Reverse transcription-quantitative polymerase chain reaction (qRT-PCR) and Western blotting analysis were used to assess the mRNA expression of TUG1 and protein expression levels of Nrf2 pathway members, respectively. The migration, invasion, and proliferation abilities of cells were assessed by the wound-healing, Transwell migration/invasion, and CCK8 assays, respectively. TUG1 was strikingly upregulated in PCa cells compared with non-tumorigenic human prostate epithelial cells. The LncTar Web Server, which is a bioinformatics tool, was used to predict the target association between TUG1 and Nrf2. Moreover, the expression of TUG1 showed a strikingly positive correlation with that of Nrf2 in TCGA PCa RNA-Seq data (r = 0.26,P = 4.63E-09). Subsequently, inhibition of TUG1 using siRNA resulted in deceased proliferation, migration, and invasion of PCa cells; however, these effects were reversed by treatment with oltipraz (an activator of Nrf2). Finally, we evaluated the Nrf2 pathway to reveal the underlying mechanism of TUG1 in PCa cells, and found that TUG1 knockdown decreased the protein expression of Nrf2 downstream members (e.g., HO-1, FTH1, and NQO1). 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However, the biological function underlying the effect of lncRNA TUG1 in PCa remains unclear. Reverse transcription-quantitative polymerase chain reaction (qRT-PCR) and Western blotting analysis were used to assess the mRNA expression of TUG1 and protein expression levels of Nrf2 pathway members, respectively. The migration, invasion, and proliferation abilities of cells were assessed by the wound-healing, Transwell migration/invasion, and CCK8 assays, respectively. TUG1 was strikingly upregulated in PCa cells compared with non-tumorigenic human prostate epithelial cells. The LncTar Web Server, which is a bioinformatics tool, was used to predict the target association between TUG1 and Nrf2. Moreover, the expression of TUG1 showed a strikingly positive correlation with that of Nrf2 in TCGA PCa RNA-Seq data (r = 0.26,P = 4.63E-09). Subsequently, inhibition of TUG1 using siRNA resulted in deceased proliferation, migration, and invasion of PCa cells; however, these effects were reversed by treatment with oltipraz (an activator of Nrf2). Finally, we evaluated the Nrf2 pathway to reveal the underlying mechanism of TUG1 in PCa cells, and found that TUG1 knockdown decreased the protein expression of Nrf2 downstream members (e.g., HO-1, FTH1, and NQO1). 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However, the biological function underlying the effect of lncRNA TUG1 in PCa remains unclear. Reverse transcription-quantitative polymerase chain reaction (qRT-PCR) and Western blotting analysis were used to assess the mRNA expression of TUG1 and protein expression levels of Nrf2 pathway members, respectively. The migration, invasion, and proliferation abilities of cells were assessed by the wound-healing, Transwell migration/invasion, and CCK8 assays, respectively. TUG1 was strikingly upregulated in PCa cells compared with non-tumorigenic human prostate epithelial cells. The LncTar Web Server, which is a bioinformatics tool, was used to predict the target association between TUG1 and Nrf2. Moreover, the expression of TUG1 showed a strikingly positive correlation with that of Nrf2 in TCGA PCa RNA-Seq data (r = 0.26,P = 4.63E-09). Subsequently, inhibition of TUG1 using siRNA resulted in deceased proliferation, migration, and invasion of PCa cells; however, these effects were reversed by treatment with oltipraz (an activator of Nrf2). Finally, we evaluated the Nrf2 pathway to reveal the underlying mechanism of TUG1 in PCa cells, and found that TUG1 knockdown decreased the protein expression of Nrf2 downstream members (e.g., HO-1, FTH1, and NQO1). LncRNA TUG1 plays an oncogenic role in human PCa cells by promoting the cell proliferation and invasion in PCa cell lines, at least partly via the Nrf2 signaling pathway.</abstract><cop>Germany</cop><pub>Elsevier GmbH</pub><pmid>32057513</pmid><doi>10.1016/j.prp.2020.152851</doi><tpages>1</tpages></addata></record>
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subjects Cell Movement - genetics
Cell Proliferation - genetics
Gene Expression Regulation, Neoplastic - genetics
Humans
Invasion
Male
Migration
Neoplasm Invasiveness - genetics
NF-E2-Related Factor 2 - genetics
NF-E2-Related Factor 2 - metabolism
NRF2
Proliferation
Prostate cancer
Prostatic Neoplasms - genetics
Prostatic Neoplasms - metabolism
Prostatic Neoplasms - pathology
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Signal Transduction - physiology
TUG1
title Long noncoding RNA TUG1 regulates prostate cancer cell proliferation, invasion and migration via the Nrf2 signaling axis
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