RP11‐367G18.1 V2 enhances clear cell renal cell carcinoma progression via induction of epithelial–mesenchymal transition
Purpose Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic microenvironment is a common feature in ccRCC and plays an essential role in the regulation of epithelial–mesenchymal transition (EMT). Acc...
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| Published in: | Cancer medicine (Malden, MA) Vol. 12; no. 8; pp. 9788 - 9801 |
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| Main Authors: | , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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United States
John Wiley & Sons, Inc
01-04-2023
John Wiley and Sons Inc Wiley |
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| Abstract | Purpose
Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic microenvironment is a common feature in ccRCC and plays an essential role in the regulation of epithelial–mesenchymal transition (EMT). Accumulating evidence manifests that long non‐coding RNAs (lncRNAs) participate in RCC tumorigenesis and regulate hypoxia‐induced EMT. Here, we identified a lncRNA RP11‐367G18.1 induced by hypoxia, that was overexpressed in ccRCC tissues.
Methods
A total of 216 specimens, including 149 ccRCC tumor samples and 67 related normal kidney parenchyma tissue samples, were collected. To investigate the biological fucntions of RP11.367G18.1 in ccRCC, migration, invasion, soft agar colony formation, xenograft tumorigenicity assays, and tail vein and orthotopic metastatic mouse models were performed. The relationship between RP11‐367G18.1 and downstream signaling was analyzed utilizing reporter assay, RNA pull‐down, chromatin immunopreciptation, and chromatin isolation by RNA purification assays.
Results
Hypoxic conditions and overexpression of HIF‐1α increased the level of RP11‐367G18.1. RP11‐367G18.1 induced EMT and enhanced cell migration and invasion through variant 2. Inhibition of RP11‐367G18.1 variant 2 reversed hypoxia‐induced EMT phenotypes. An in vivo study revealed that RP11‐367G18.1 variant 2 was required for hypoxia‐induced tumor growth and metastasis in ccRCC. Mechanistically, RP11‐367G18.1 variant 2 interacted with p300 histone acetyltransferase to regulate lysine 16 acetylation on histone 4 (H4K16Ac), thus contributing to hypoxia‐regulated gene expression. Clinically, RP11‐367G18.1 variant 2 was upregulated in ccRCC tissues, particularly metastatic ccRCC tissues, and it is linked to poor overall survival.
Conclusion
These findings demonstrate the prognostic value and EMT‐promoting role of RP11‐367G18.1 and indicate that this lncRNA may provide a therapeutic target for ccRCC.
Hypoxia upregulated lncRNA RP11‐367G18.1 variant 2 which was associated with p300‐mediated chromatin modifying complex to activate H4K16Ac marks. RP11‐367G18.1 variant 2 increased the levels of H4K16Ac on the promoter of hypoxia‐regulated genes leading to EMT and tumor metastasis. |
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| AbstractList | PURPOSEMetastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic microenvironment is a common feature in ccRCC and plays an essential role in the regulation of epithelial-mesenchymal transition (EMT). Accumulating evidence manifests that long non-coding RNAs (lncRNAs) participate in RCC tumorigenesis and regulate hypoxia-induced EMT. Here, we identified a lncRNA RP11-367G18.1 induced by hypoxia, that was overexpressed in ccRCC tissues. METHODSA total of 216 specimens, including 149 ccRCC tumor samples and 67 related normal kidney parenchyma tissue samples, were collected. To investigate the biological fucntions of RP11.367G18.1 in ccRCC, migration, invasion, soft agar colony formation, xenograft tumorigenicity assays, and tail vein and orthotopic metastatic mouse models were performed. The relationship between RP11-367G18.1 and downstream signaling was analyzed utilizing reporter assay, RNA pull-down, chromatin immunopreciptation, and chromatin isolation by RNA purification assays. RESULTSHypoxic conditions and overexpression of HIF-1α increased the level of RP11-367G18.1. RP11-367G18.1 induced EMT and enhanced cell migration and invasion through variant 2. Inhibition of RP11-367G18.1 variant 2 reversed hypoxia-induced EMT phenotypes. An in vivo study revealed that RP11-367G18.1 variant 2 was required for hypoxia-induced tumor growth and metastasis in ccRCC. Mechanistically, RP11-367G18.1 variant 2 interacted with p300 histone acetyltransferase to regulate lysine 16 acetylation on histone 4 (H4K16Ac), thus contributing to hypoxia-regulated gene expression. Clinically, RP11-367G18.1 variant 2 was upregulated in ccRCC tissues, particularly metastatic ccRCC tissues, and it is linked to poor overall survival. CONCLUSIONThese findings demonstrate the prognostic value and EMT-promoting role of RP11-367G18.1 and indicate that this lncRNA may provide a therapeutic target for ccRCC. Abstract Purpose Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic microenvironment is a common feature in ccRCC and plays an essential role in the regulation of epithelial–mesenchymal transition (EMT). Accumulating evidence manifests that long non‐coding RNAs (lncRNAs) participate in RCC tumorigenesis and regulate hypoxia‐induced EMT. Here, we identified a lncRNA RP11‐367G18.1 induced by hypoxia, that was overexpressed in ccRCC tissues. Methods A total of 216 specimens, including 149 ccRCC tumor samples and 67 related normal kidney parenchyma tissue samples, were collected. To investigate the biological fucntions of RP11.367G18.1 in ccRCC, migration, invasion, soft agar colony formation, xenograft tumorigenicity assays, and tail vein and orthotopic metastatic mouse models were performed. The relationship between RP11‐367G18.1 and downstream signaling was analyzed utilizing reporter assay, RNA pull‐down, chromatin immunopreciptation, and chromatin isolation by RNA purification assays. Results Hypoxic conditions and overexpression of HIF‐1α increased the level of RP11‐367G18.1. RP11‐367G18.1 induced EMT and enhanced cell migration and invasion through variant 2. Inhibition of RP11‐367G18.1 variant 2 reversed hypoxia‐induced EMT phenotypes. An in vivo study revealed that RP11‐367G18.1 variant 2 was required for hypoxia‐induced tumor growth and metastasis in ccRCC. Mechanistically, RP11‐367G18.1 variant 2 interacted with p300 histone acetyltransferase to regulate lysine 16 acetylation on histone 4 (H4K16Ac), thus contributing to hypoxia‐regulated gene expression. Clinically, RP11‐367G18.1 variant 2 was upregulated in ccRCC tissues, particularly metastatic ccRCC tissues, and it is linked to poor overall survival. Conclusion These findings demonstrate the prognostic value and EMT‐promoting role of RP11‐367G18.1 and indicate that this lncRNA may provide a therapeutic target for ccRCC. Abstract Purpose Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic microenvironment is a common feature in ccRCC and plays an essential role in the regulation of epithelial–mesenchymal transition (EMT). Accumulating evidence manifests that long non‐coding RNAs (lncRNAs) participate in RCC tumorigenesis and regulate hypoxia‐induced EMT. Here, we identified a lncRNA RP11‐367G18.1 induced by hypoxia, that was overexpressed in ccRCC tissues. Methods A total of 216 specimens, including 149 ccRCC tumor samples and 67 related normal kidney parenchyma tissue samples, were collected. To investigate the biological fucntions of RP11.367G18.1 in ccRCC, migration, invasion, soft agar colony formation, xenograft tumorigenicity assays, and tail vein and orthotopic metastatic mouse models were performed. The relationship between RP11‐367G18.1 and downstream signaling was analyzed utilizing reporter assay, RNA pull‐down, chromatin immunopreciptation, and chromatin isolation by RNA purification assays. Results Hypoxic conditions and overexpression of HIF‐1α increased the level of RP11‐367G18.1 . RP11‐367G18.1 induced EMT and enhanced cell migration and invasion through variant 2. Inhibition of RP11‐367G18.1 variant 2 reversed hypoxia‐induced EMT phenotypes. An in vivo study revealed that RP11‐367G18.1 variant 2 was required for hypoxia‐induced tumor growth and metastasis in ccRCC. Mechanistically, RP11‐367G18.1 variant 2 interacted with p300 histone acetyltransferase to regulate lysine 16 acetylation on histone 4 (H4K16Ac), thus contributing to hypoxia‐regulated gene expression. Clinically, RP11‐367G18.1 variant 2 was upregulated in ccRCC tissues, particularly metastatic ccRCC tissues, and it is linked to poor overall survival. Conclusion These findings demonstrate the prognostic value and EMT‐promoting role of RP11‐367G18.1 and indicate that this lncRNA may provide a therapeutic target for ccRCC. Hypoxia upregulated lncRNA RP11‐367G18.1 variant 2 which was associated with p300‐mediated chromatin modifying complex to activate H4K16Ac marks. RP11‐367G18.1 variant 2 increased the levels of H4K16Ac on the promoter of hypoxia‐regulated genes leading to EMT and tumor metastasis. Purpose Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic microenvironment is a common feature in ccRCC and plays an essential role in the regulation of epithelial–mesenchymal transition (EMT). Accumulating evidence manifests that long non‐coding RNAs (lncRNAs) participate in RCC tumorigenesis and regulate hypoxia‐induced EMT. Here, we identified a lncRNA RP11‐367G18.1 induced by hypoxia, that was overexpressed in ccRCC tissues. Methods A total of 216 specimens, including 149 ccRCC tumor samples and 67 related normal kidney parenchyma tissue samples, were collected. To investigate the biological fucntions of RP11.367G18.1 in ccRCC, migration, invasion, soft agar colony formation, xenograft tumorigenicity assays, and tail vein and orthotopic metastatic mouse models were performed. The relationship between RP11‐367G18.1 and downstream signaling was analyzed utilizing reporter assay, RNA pull‐down, chromatin immunopreciptation, and chromatin isolation by RNA purification assays. Results Hypoxic conditions and overexpression of HIF‐1α increased the level of RP11‐367G18.1. RP11‐367G18.1 induced EMT and enhanced cell migration and invasion through variant 2. Inhibition of RP11‐367G18.1 variant 2 reversed hypoxia‐induced EMT phenotypes. An in vivo study revealed that RP11‐367G18.1 variant 2 was required for hypoxia‐induced tumor growth and metastasis in ccRCC. Mechanistically, RP11‐367G18.1 variant 2 interacted with p300 histone acetyltransferase to regulate lysine 16 acetylation on histone 4 (H4K16Ac), thus contributing to hypoxia‐regulated gene expression. Clinically, RP11‐367G18.1 variant 2 was upregulated in ccRCC tissues, particularly metastatic ccRCC tissues, and it is linked to poor overall survival. Conclusion These findings demonstrate the prognostic value and EMT‐promoting role of RP11‐367G18.1 and indicate that this lncRNA may provide a therapeutic target for ccRCC. Hypoxia upregulated lncRNA RP11‐367G18.1 variant 2 which was associated with p300‐mediated chromatin modifying complex to activate H4K16Ac marks. RP11‐367G18.1 variant 2 increased the levels of H4K16Ac on the promoter of hypoxia‐regulated genes leading to EMT and tumor metastasis. Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic microenvironment is a common feature in ccRCC and plays an essential role in the regulation of epithelial-mesenchymal transition (EMT). Accumulating evidence manifests that long non-coding RNAs (lncRNAs) participate in RCC tumorigenesis and regulate hypoxia-induced EMT. Here, we identified a lncRNA RP11-367G18.1 induced by hypoxia, that was overexpressed in ccRCC tissues. A total of 216 specimens, including 149 ccRCC tumor samples and 67 related normal kidney parenchyma tissue samples, were collected. To investigate the biological fucntions of RP11.367G18.1 in ccRCC, migration, invasion, soft agar colony formation, xenograft tumorigenicity assays, and tail vein and orthotopic metastatic mouse models were performed. The relationship between RP11-367G18.1 and downstream signaling was analyzed utilizing reporter assay, RNA pull-down, chromatin immunopreciptation, and chromatin isolation by RNA purification assays. Hypoxic conditions and overexpression of HIF-1α increased the level of RP11-367G18.1. RP11-367G18.1 induced EMT and enhanced cell migration and invasion through variant 2. Inhibition of RP11-367G18.1 variant 2 reversed hypoxia-induced EMT phenotypes. An in vivo study revealed that RP11-367G18.1 variant 2 was required for hypoxia-induced tumor growth and metastasis in ccRCC. Mechanistically, RP11-367G18.1 variant 2 interacted with p300 histone acetyltransferase to regulate lysine 16 acetylation on histone 4 (H4K16Ac), thus contributing to hypoxia-regulated gene expression. Clinically, RP11-367G18.1 variant 2 was upregulated in ccRCC tissues, particularly metastatic ccRCC tissues, and it is linked to poor overall survival. These findings demonstrate the prognostic value and EMT-promoting role of RP11-367G18.1 and indicate that this lncRNA may provide a therapeutic target for ccRCC. |
| Author | Wu, Han‐Tsang Hsu, Kai‐Wen Shao, I‐Hung Chen, Ji‐Lin Lai, Joseph Chieh‐Yu Wu, Kou‐Juey Wu, Heng‐Hsiung Chang, Jeng‐Shou Pang, See‐Tong Peng, Pei‐Hua |
| AuthorAffiliation | 9 Institute of Biomedical Science China Medical University Taichung Taiwan 3 Graduate Institute of Clinical Medical Sciences College of Medicine, Chang Gung University Taoyuan Taiwan 4 Department of Medicine College of Medicine, Chang Gung University Taoyuan Taiwan 6 Program for Cancer Biology and Drug Discovery China Medical University Taichung City Taiwan 1 Cancer Genome Research Center Chang Gung Memorial Hospital at Linkou Taoyuan Taiwan 10 Cancer Research Center Changhua Christian Hospital Changhua Taiwan 13 Institute of Translational Medicine and New Drug Development China Medical University Taichung City Taiwan 2 Division of Urology, Department of Surgery Chang Gung Memorial Hospital at Linkou Taoyuan Taiwan 8 Comprehensive Breast Health Center Taipei Veterans General Hospital Taipei Taiwan 12 Institute of Clinical Medical Sciences Chang Gung University Taoyuan Taiwan 5 Research Center for Cancer Biology China Medical University Taichung City Taiwan 7 Drug Development Center China Medical |
| AuthorAffiliation_xml | – name: 3 Graduate Institute of Clinical Medical Sciences College of Medicine, Chang Gung University Taoyuan Taiwan – name: 10 Cancer Research Center Changhua Christian Hospital Changhua Taiwan – name: 1 Cancer Genome Research Center Chang Gung Memorial Hospital at Linkou Taoyuan Taiwan – name: 9 Institute of Biomedical Science China Medical University Taichung Taiwan – name: 7 Drug Development Center China Medical University Taichung City Taiwan – name: 11 Institute of Cellular and Organismic Biology Academia Sinica Taipei Taiwan – name: 5 Research Center for Cancer Biology China Medical University Taichung City Taiwan – name: 8 Comprehensive Breast Health Center Taipei Veterans General Hospital Taipei Taiwan – name: 6 Program for Cancer Biology and Drug Discovery China Medical University Taichung City Taiwan – name: 4 Department of Medicine College of Medicine, Chang Gung University Taoyuan Taiwan – name: 12 Institute of Clinical Medical Sciences Chang Gung University Taoyuan Taiwan – name: 13 Institute of Translational Medicine and New Drug Development China Medical University Taichung City Taiwan – name: 2 Division of Urology, Department of Surgery Chang Gung Memorial Hospital at Linkou Taoyuan Taiwan |
| Author_xml | – sequence: 1 givenname: I‐Hung surname: Shao fullname: Shao, I‐Hung organization: College of Medicine, Chang Gung University – sequence: 2 givenname: Pei‐Hua surname: Peng fullname: Peng, Pei‐Hua organization: Chang Gung Memorial Hospital at Linkou – sequence: 3 givenname: Heng‐Hsiung surname: Wu fullname: Wu, Heng‐Hsiung organization: China Medical University – sequence: 4 givenname: Ji‐Lin surname: Chen fullname: Chen, Ji‐Lin organization: Taipei Veterans General Hospital – sequence: 5 givenname: Joseph Chieh‐Yu surname: Lai fullname: Lai, Joseph Chieh‐Yu organization: China Medical University – sequence: 6 givenname: Jeng‐Shou surname: Chang fullname: Chang, Jeng‐Shou organization: Chang Gung Memorial Hospital at Linkou – sequence: 7 givenname: Han‐Tsang surname: Wu fullname: Wu, Han‐Tsang organization: Changhua Christian Hospital – sequence: 8 givenname: Kou‐Juey surname: Wu fullname: Wu, Kou‐Juey organization: Chang Gung University – sequence: 9 givenname: See‐Tong surname: Pang fullname: Pang, See‐Tong email: pst64lab@gmail.com organization: College of Medicine, Chang Gung University – sequence: 10 givenname: Kai‐Wen orcidid: 0000-0002-9736-8869 surname: Hsu fullname: Hsu, Kai‐Wen email: kwhsu@mail.cmu.edu.tw organization: China Medical University |
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| Copyright | 2023 The Authors. published by John Wiley & Sons Ltd. 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | hypoxia H4K16Ac epithelial-mesenchymal transition clear cell renal cell carcinoma lncRNA RP11-367G18.1 |
| Language | English |
| License | Attribution 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| Notes | I‐Hung Shao, Pei‐Hua Peng, Heng‐Hsiung Wu, and Ji‐Lin Chen contributed equally to this study. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The... Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic... Abstract Purpose Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype.... PurposeMetastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic... PURPOSEMetastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype. The hypoxic... Hypoxia upregulated lncRNA RP11‐367G18.1 variant 2 which was associated with p300‐mediated chromatin modifying complex to activate H4K16Ac marks. RP11‐367G18.1... Abstract Purpose Metastasis is the end stage of renal cell carcinoma (RCC), and clear cell renal cell carcinoma (ccRCC) is the most common malignant subtype.... |
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| SubjectTerms | Acetylation Animal models Animals Biomarkers Carcinoma - genetics Carcinoma, Renal Cell - pathology Cell culture Cell Line, Tumor Cell migration Cell Movement - genetics Cell Proliferation - genetics Chromatin clear cell renal cell carcinoma Clear cell-type renal cell carcinoma Epigenetics Epithelial-Mesenchymal Transition - genetics epithelial–mesenchymal transition Gene expression Gene Expression Regulation, Neoplastic Growth models H4K16Ac Histone acetyltransferase Humans Hypoxia Hypoxia - genetics Hypoxia-inducible factor 1a Kidney cancer Kidney Neoplasms - pathology lncRNA RP11‐367G18.1 Medical prognosis Metastases Metastasis Mice Microenvironments Non-coding RNA Parenchyma Phenotypes Plasmids RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Therapeutic targets Transcription factors Tumor Microenvironment Tumorigenesis Tumorigenicity Tumors |
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| Title | RP11‐367G18.1 V2 enhances clear cell renal cell carcinoma progression via induction of epithelial–mesenchymal transition |
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