lncRNA FGD5-AS1 is required for gastric cancer proliferation by inhibiting cell senescence and ROS production via stabilizing YBX1
The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA, FGD5-AS1's non-ceRNA biological function in cancer is unclear. RNA-seq studies and chromatin immunoprecipitation (Chip) assays were performe...
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Published in | Journal of experimental & clinical cancer research Vol. 43; no. 1; pp. 188 - 17 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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BioMed Central Ltd
05.07.2024
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Abstract | The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA, FGD5-AS1's non-ceRNA biological function in cancer is unclear.
RNA-seq studies and chromatin immunoprecipitation (Chip) assays were performed to identify ZEB1-regulated lncRNAs. RNA sequencing, RNA pulldown, RNA Immunoprecipitation assays, and rescue assays were conducted to explore the molecular mechanisms of FGD5-AS1 in GC.
As one of the most abundant lncRNAs in cells, FGD5-AS1 has been shown to be transcriptionally activated by ZEB1, thus closely related to epithelial-mesenchymal transition (EMT) signaling. Clinical analysis showed that FGD5-AS1 overexpression was clinically associated with lymph node metastasis, and predicted poor survival in GC. Loss-of-function studies confirmed that FGD5-AS1 knockdown inhibited GC proliferation and induced cisplatin chemosensibility, cell senescence, and DNA damage in GC cells. Mechanismically, FGD5-AS1 is a YBX1-binding lncRNA due to its mRNA contains three adjacent structural motifs (UAAUCCCA, ACCAGCCU, and CAGUGAGC) that can be recognized and bound by YBX1. And this RNA-protein interaction prolonged the half-life of the YBX1 protein in GC. Additionally, a rescue assay showed that FGD5-AS1 promotes GC by repressing cell senescence and ROS production via YBX1.
FGD5-AS1 is a cellular high-abundant lncRNA that is transcriptionally regulated by ZEB1. FGD5-AS1 overexpression promoted GC progression by inhibiting cell senescence and ROS production through binding and stabilizing the YBX1 protein. |
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AbstractList | Abstract Background The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA, FGD5-AS1’s non-ceRNA biological function in cancer is unclear. Methods RNA-seq studies and chromatin immunoprecipitation (Chip) assays were performed to identify ZEB1-regulated lncRNAs. RNA sequencing, RNA pulldown, RNA Immunoprecipitation assays, and rescue assays were conducted to explore the molecular mechanisms of FGD5-AS1 in GC. Results As one of the most abundant lncRNAs in cells, FGD5-AS1 has been shown to be transcriptionally activated by ZEB1, thus closely related to epithelial-mesenchymal transition (EMT) signaling. Clinical analysis showed that FGD5-AS1 overexpression was clinically associated with lymph node metastasis, and predicted poor survival in GC. Loss-of-function studies confirmed that FGD5-AS1 knockdown inhibited GC proliferation and induced cisplatin chemosensibility, cell senescence, and DNA damage in GC cells. Mechanismically, FGD5-AS1 is a YBX1-binding lncRNA due to its mRNA contains three adjacent structural motifs (UAAUCCCA, ACCAGCCU, and CAGUGAGC) that can be recognized and bound by YBX1. And this RNA-protein interaction prolonged the half-life of the YBX1 protein in GC. Additionally, a rescue assay showed that FGD5-AS1 promotes GC by repressing cell senescence and ROS production via YBX1. Conclusion FGD5-AS1 is a cellular high-abundant lncRNA that is transcriptionally regulated by ZEB1. FGD5-AS1 overexpression promoted GC progression by inhibiting cell senescence and ROS production through binding and stabilizing the YBX1 protein. Background The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA, FGD5-AS1's non-ceRNA biological function in cancer is unclear. Methods RNA-seq studies and chromatin immunoprecipitation (Chip) assays were performed to identify ZEB1-regulated lncRNAs. RNA sequencing, RNA pulldown, RNA Immunoprecipitation assays, and rescue assays were conducted to explore the molecular mechanisms of FGD5-AS1 in GC. Results As one of the most abundant lncRNAs in cells, FGD5-AS1 has been shown to be transcriptionally activated by ZEB1, thus closely related to epithelial-mesenchymal transition (EMT) signaling. Clinical analysis showed that FGD5-AS1 overexpression was clinically associated with lymph node metastasis, and predicted poor survival in GC. Loss-of-function studies confirmed that FGD5-AS1 knockdown inhibited GC proliferation and induced cisplatin chemosensibility, cell senescence, and DNA damage in GC cells. Mechanismically, FGD5-AS1 is a YBX1-binding lncRNA due to its mRNA contains three adjacent structural motifs (UAAUCCCA, ACCAGCCU, and CAGUGAGC) that can be recognized and bound by YBX1. And this RNA-protein interaction prolonged the half-life of the YBX1 protein in GC. Additionally, a rescue assay showed that FGD5-AS1 promotes GC by repressing cell senescence and ROS production via YBX1. Conclusion FGD5-AS1 is a cellular high-abundant lncRNA that is transcriptionally regulated by ZEB1. FGD5-AS1 overexpression promoted GC progression by inhibiting cell senescence and ROS production through binding and stabilizing the YBX1 protein. Keywords: Cell senescence, ROS, Transcriptional regulation, RNA-protein interaction, Gastric cancer The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA, FGD5-AS1's non-ceRNA biological function in cancer is unclear.BACKGROUNDThe vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA, FGD5-AS1's non-ceRNA biological function in cancer is unclear.RNA-seq studies and chromatin immunoprecipitation (Chip) assays were performed to identify ZEB1-regulated lncRNAs. RNA sequencing, RNA pulldown, RNA Immunoprecipitation assays, and rescue assays were conducted to explore the molecular mechanisms of FGD5-AS1 in GC.METHODSRNA-seq studies and chromatin immunoprecipitation (Chip) assays were performed to identify ZEB1-regulated lncRNAs. RNA sequencing, RNA pulldown, RNA Immunoprecipitation assays, and rescue assays were conducted to explore the molecular mechanisms of FGD5-AS1 in GC.As one of the most abundant lncRNAs in cells, FGD5-AS1 has been shown to be transcriptionally activated by ZEB1, thus closely related to epithelial-mesenchymal transition (EMT) signaling. Clinical analysis showed that FGD5-AS1 overexpression was clinically associated with lymph node metastasis, and predicted poor survival in GC. Loss-of-function studies confirmed that FGD5-AS1 knockdown inhibited GC proliferation and induced cisplatin chemosensibility, cell senescence, and DNA damage in GC cells. Mechanismically, FGD5-AS1 is a YBX1-binding lncRNA due to its mRNA contains three adjacent structural motifs (UAAUCCCA, ACCAGCCU, and CAGUGAGC) that can be recognized and bound by YBX1. And this RNA-protein interaction prolonged the half-life of the YBX1 protein in GC. Additionally, a rescue assay showed that FGD5-AS1 promotes GC by repressing cell senescence and ROS production via YBX1.RESULTSAs one of the most abundant lncRNAs in cells, FGD5-AS1 has been shown to be transcriptionally activated by ZEB1, thus closely related to epithelial-mesenchymal transition (EMT) signaling. Clinical analysis showed that FGD5-AS1 overexpression was clinically associated with lymph node metastasis, and predicted poor survival in GC. Loss-of-function studies confirmed that FGD5-AS1 knockdown inhibited GC proliferation and induced cisplatin chemosensibility, cell senescence, and DNA damage in GC cells. Mechanismically, FGD5-AS1 is a YBX1-binding lncRNA due to its mRNA contains three adjacent structural motifs (UAAUCCCA, ACCAGCCU, and CAGUGAGC) that can be recognized and bound by YBX1. And this RNA-protein interaction prolonged the half-life of the YBX1 protein in GC. Additionally, a rescue assay showed that FGD5-AS1 promotes GC by repressing cell senescence and ROS production via YBX1.FGD5-AS1 is a cellular high-abundant lncRNA that is transcriptionally regulated by ZEB1. FGD5-AS1 overexpression promoted GC progression by inhibiting cell senescence and ROS production through binding and stabilizing the YBX1 protein.CONCLUSIONFGD5-AS1 is a cellular high-abundant lncRNA that is transcriptionally regulated by ZEB1. FGD5-AS1 overexpression promoted GC progression by inhibiting cell senescence and ROS production through binding and stabilizing the YBX1 protein. The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA, FGD5-AS1's non-ceRNA biological function in cancer is unclear. RNA-seq studies and chromatin immunoprecipitation (Chip) assays were performed to identify ZEB1-regulated lncRNAs. RNA sequencing, RNA pulldown, RNA Immunoprecipitation assays, and rescue assays were conducted to explore the molecular mechanisms of FGD5-AS1 in GC. As one of the most abundant lncRNAs in cells, FGD5-AS1 has been shown to be transcriptionally activated by ZEB1, thus closely related to epithelial-mesenchymal transition (EMT) signaling. Clinical analysis showed that FGD5-AS1 overexpression was clinically associated with lymph node metastasis, and predicted poor survival in GC. Loss-of-function studies confirmed that FGD5-AS1 knockdown inhibited GC proliferation and induced cisplatin chemosensibility, cell senescence, and DNA damage in GC cells. Mechanismically, FGD5-AS1 is a YBX1-binding lncRNA due to its mRNA contains three adjacent structural motifs (UAAUCCCA, ACCAGCCU, and CAGUGAGC) that can be recognized and bound by YBX1. And this RNA-protein interaction prolonged the half-life of the YBX1 protein in GC. Additionally, a rescue assay showed that FGD5-AS1 promotes GC by repressing cell senescence and ROS production via YBX1. FGD5-AS1 is a cellular high-abundant lncRNA that is transcriptionally regulated by ZEB1. FGD5-AS1 overexpression promoted GC progression by inhibiting cell senescence and ROS production through binding and stabilizing the YBX1 protein. The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA, FGD5-AS1's non-ceRNA biological function in cancer is unclear. RNA-seq studies and chromatin immunoprecipitation (Chip) assays were performed to identify ZEB1-regulated lncRNAs. RNA sequencing, RNA pulldown, RNA Immunoprecipitation assays, and rescue assays were conducted to explore the molecular mechanisms of FGD5-AS1 in GC. As one of the most abundant lncRNAs in cells, FGD5-AS1 has been shown to be transcriptionally activated by ZEB1, thus closely related to epithelial-mesenchymal transition (EMT) signaling. Clinical analysis showed that FGD5-AS1 overexpression was clinically associated with lymph node metastasis, and predicted poor survival in GC. Loss-of-function studies confirmed that FGD5-AS1 knockdown inhibited GC proliferation and induced cisplatin chemosensibility, cell senescence, and DNA damage in GC cells. Mechanismically, FGD5-AS1 is a YBX1-binding lncRNA due to its mRNA contains three adjacent structural motifs (UAAUCCCA, ACCAGCCU, and CAGUGAGC) that can be recognized and bound by YBX1. And this RNA-protein interaction prolonged the half-life of the YBX1 protein in GC. Additionally, a rescue assay showed that FGD5-AS1 promotes GC by repressing cell senescence and ROS production via YBX1. FGD5-AS1 is a cellular high-abundant lncRNA that is transcriptionally regulated by ZEB1. FGD5-AS1 overexpression promoted GC progression by inhibiting cell senescence and ROS production through binding and stabilizing the YBX1 protein. FGD5-AS1 is an EMT-related, cellularly abundant lncRNA. The expression of FGD5-AS1 is directly regulated by the transcription factor ZEB1. FGD5-AS1 overexpression was clinically associated with lymph node metastasis and a poor prognosis in GC. Knockdown of FGD5-AS1 causes senescence-associated secretory phenotypes, DNA damage, cisplatin chemosensibility, and growth inhibition in GC cells. FGD5-AS1 prolongs the half-life of the YBX1 protein by RNA-protein interaction. The UAAUCCCA, ACCAGCCU, and CAGUGAGC linear 8-mer motifs in the FGD5-AS1 transcript mediate the interaction between YBX1 and FGD5-AS1. FGD5-AS1 promotes GC proliferation by inhibiting cell senescence and ROS production in a YBX1-dependent manner. FGD5-AS1 is an EMT-related, cellularly abundant lncRNA. The expression of FGD5-AS1 is directly regulated by the transcription factor ZEB1.FGD5-AS1 overexpression was clinically associated with lymph node metastasis and a poor prognosis in GC.Knockdown of FGD5-AS1 causes senescence-associated secretory phenotypes, DNA damage, cisplatin chemosensibility, and growth inhibition in GC cells.FGD5-AS1 prolongs the half-life of the YBX1 protein by RNA-protein interaction. The UAAUCCCA, ACCAGCCU, and CAGUGAGC linear 8-mer motifs in the FGD5-AS1 transcript mediate the interaction between YBX1 and FGD5-AS1.FGD5-AS1 promotes GC proliferation by inhibiting cell senescence and ROS production in a YBX1-dependent manner. |
ArticleNumber | 188 |
Audience | Academic |
Author | Huang, Pan Zhang, Xiangang Liu, Yue Xia, Lingyun Qin, Shanshan Leng, Weidong Li, Dandan |
Author_xml | – sequence: 1 givenname: Shanshan orcidid: 0000-0002-8527-5278 surname: Qin fullname: Qin, Shanshan email: qinss77@163.com, qinss77@163.com, qinss77@163.com organization: Shiyan Key Laboratory of Natural Medicine Nanoformulation Research, Hubei University of Medicine, Shiyan, Hubei, 442000, China. qinss77@163.com – sequence: 2 givenname: Yue surname: Liu fullname: Liu, Yue organization: Laboratory of Tumor Biology, Academy of Bio-Medicine Research, Hubei University of Medicine, Shiyan, Hubei, P.R. China – sequence: 3 givenname: Xiangang surname: Zhang fullname: Zhang, Xiangang organization: Laboratory of Tumor Biology, Academy of Bio-Medicine Research, Hubei University of Medicine, Shiyan, Hubei, P.R. China – sequence: 4 givenname: Pan surname: Huang fullname: Huang, Pan organization: Laboratory of Tumor Biology, Academy of Bio-Medicine Research, Hubei University of Medicine, Shiyan, Hubei, P.R. China – sequence: 5 givenname: Lingyun surname: Xia fullname: Xia, Lingyun organization: Department of Stomatology, Taihe Hospital and Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei, 442000, China – sequence: 6 givenname: Weidong surname: Leng fullname: Leng, Weidong email: lwd35@163.com organization: Department of Stomatology, Taihe Hospital and Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei, 442000, China. lwd35@163.com – sequence: 7 givenname: Dandan surname: Li fullname: Li, Dandan email: lidandan_cup@163.com, lidandan_cup@163.com, lidandan_cup@163.com organization: Shiyan Key Laboratory of Natural Medicine Nanoformulation Research, Hubei University of Medicine, Shiyan, Hubei, 442000, China. lidandan_cup@163.com |
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Keywords | Cell senescence RNA-protein interaction Transcriptional regulation Gastric cancer ROS |
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Snippet | The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance lncRNA,... Abstract Background The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression... Background The vast majority of lncRNAs have low expression abundance, which greatly limits their functional range and impact. As a high expression abundance... FGD5-AS1 is an EMT-related, cellularly abundant lncRNA. The expression of FGD5-AS1 is directly regulated by the transcription factor ZEB1.FGD5-AS1... FGD5-AS1 is an EMT-related, cellularly abundant lncRNA. The expression of FGD5-AS1 is directly regulated by the transcription factor ZEB1. FGD5-AS1... |
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SubjectTerms | Analysis Animals Apoptosis Biomarkers Cancer Cancer therapies Cell growth Cell Line, Tumor Cell Proliferation Cell senescence Cellular Senescence Chromatin Development and progression Epithelial-Mesenchymal Transition Female Gastric cancer Gene Expression Regulation, Neoplastic Genes Genetic transcription Guanine Nucleotide Exchange Factors Humans Lymphatic system Male Medical prognosis Messenger RNA Metastasis Mice Protein binding Proteins Reactive Oxygen Species - metabolism RNA polymerase RNA sequencing RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA-protein interaction ROS Senescence Stem cells Stomach cancer Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Transcription factors Transcriptional regulation Y-Box-Binding Protein 1 - genetics Y-Box-Binding Protein 1 - metabolism |
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Title | lncRNA FGD5-AS1 is required for gastric cancer proliferation by inhibiting cell senescence and ROS production via stabilizing YBX1 |
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