Inhibition of mTORC1 by lncRNA H19 via disrupting 4E-BP1/Raptor interaction in pituitary tumours
Aberrant expression of long noncoding RNA H19 has been associated with tumour progression, but the underlying molecular tumourigenesis mechanisms remain largely unknown. Here, we report that H19 expression is frequently downregulated in human primary pituitary adenomas and is negatively correlated w...
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Published in | Nature communications Vol. 9; no. 1; pp. 4624 - 14 |
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Main Authors | , , , , , , , , , , , , , , , , , , |
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Nature Publishing Group UK
05.11.2018
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Abstract | Aberrant expression of long noncoding RNA H19 has been associated with tumour progression, but the underlying molecular tumourigenesis mechanisms remain largely unknown. Here, we report that H19 expression is frequently downregulated in human primary pituitary adenomas and is negatively correlated with tumour progression. Consistently, upregulation of H19 expression inhibits pituitary tumour cell proliferation in vitro and tumour growth in vivo. Importantly, we uncover a function of H19, which controls cell/tumour growth through inhibiting function of mTORC1 but not mTORC2. Mechanistically, we show that H19 could block mTORC1-mediated 4E-BP1 phosphorylation without affecting S6K1 activation. At the molecular level, H19 interacted with 4E-BP1 at the TOS motif and competitively inhibited 4E-BP1 binding to Raptor. Finally, we demonstrate that H19 is more effective than cabergoline treatment in the suppression of pituitary tumours. Together, our study uncovered the role of H19-mTOR-4E-BP1 axis in pituitary tumour growth regulation that may be a potential therapeutic target for human pituitary tumours.
LncRNA H19 has been shown to be aberrantly expressed in different cancers. Here, the authors show that H19 lncRNA is downregulated in pituitary adenomas and H19 is able to impede pituitary tumorigenesis via disruption of 4E-BPB1 and Raptor interaction to inhibit the phosphorylation of 4E-BP1. |
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AbstractList | Aberrant expression of long noncoding RNA H19 has been associated with tumour progression, but the underlying molecular tumourigenesis mechanisms remain largely unknown. Here, we report that H19 expression is frequently downregulated in human primary pituitary adenomas and is negatively correlated with tumour progression. Consistently, upregulation of H19 expression inhibits pituitary tumour cell proliferation in vitro and tumour growth in vivo. Importantly, we uncover a function of H19, which controls cell/tumour growth through inhibiting function of mTORC1 but not mTORC2. Mechanistically, we show that H19 could block mTORC1-mediated 4E-BP1 phosphorylation without affecting S6K1 activation. At the molecular level, H19 interacted with 4E-BP1 at the TOS motif and competitively inhibited 4E-BP1 binding to Raptor. Finally, we demonstrate that H19 is more effective than cabergoline treatment in the suppression of pituitary tumours. Together, our study uncovered the role of H19-mTOR-4E-BP1 axis in pituitary tumour growth regulation that may be a potential therapeutic target for human pituitary tumours. LncRNA H19 has been shown to be aberrantly expressed in different cancers. Here, the authors show that H19 lncRNA is downregulated in pituitary adenomas and H19 is able to impede pituitary tumorigenesis via disruption of 4E-BPB1 and Raptor interaction to inhibit the phosphorylation of 4E-BP1. Aberrant expression of long noncoding RNA H19 has been associated with tumour progression, but the underlying molecular tumourigenesis mechanisms remain largely unknown. Here, we report that H19 expression is frequently downregulated in human primary pituitary adenomas and is negatively correlated with tumour progression. Consistently, upregulation of H19 expression inhibits pituitary tumour cell proliferation in vitro and tumour growth in vivo. Importantly, we uncover a function of H19, which controls cell/tumour growth through inhibiting function of mTORC1 but not mTORC2. Mechanistically, we show that H19 could block mTORC1-mediated 4E-BP1 phosphorylation without affecting S6K1 activation. At the molecular level, H19 interacted with 4E-BP1 at the TOS motif and competitively inhibited 4E-BP1 binding to Raptor. Finally, we demonstrate that H19 is more effective than cabergoline treatment in the suppression of pituitary tumours. Together, our study uncovered the role of H19-mTOR-4E-BP1 axis in pituitary tumour growth regulation that may be a potential therapeutic target for human pituitary tumours. LncRNA H19 has been shown to be aberrantly expressed in different cancers. Here, the authors show that H19 lncRNA is downregulated in pituitary adenomas and H19 is able to impede pituitary tumorigenesis via disruption of 4E-BPB1 and Raptor interaction to inhibit the phosphorylation of 4E-BP1. Abstract Aberrant expression of long noncoding RNA H19 has been associated with tumour progression, but the underlying molecular tumourigenesis mechanisms remain largely unknown. Here, we report that H19 expression is frequently downregulated in human primary pituitary adenomas and is negatively correlated with tumour progression. Consistently, upregulation of H19 expression inhibits pituitary tumour cell proliferation in vitro and tumour growth in vivo. Importantly, we uncover a function of H19, which controls cell/tumour growth through inhibiting function of mTORC1 but not mTORC2. Mechanistically, we show that H19 could block mTORC1-mediated 4E-BP1 phosphorylation without affecting S6K1 activation. At the molecular level, H19 interacted with 4E-BP1 at the TOS motif and competitively inhibited 4E-BP1 binding to Raptor. Finally, we demonstrate that H19 is more effective than cabergoline treatment in the suppression of pituitary tumours. Together, our study uncovered the role of H19-mTOR-4E-BP1 axis in pituitary tumour growth regulation that may be a potential therapeutic target for human pituitary tumours. |
ArticleNumber | 4624 |
Author | Yan, Lichong Cai, Lin Guo, Yu Hang Wang, Yu Su, Bing Wu, Ze Rui Wei, Yong Xu Wu, Zhe Bao Liu, Yan Ting Tang, Hao Huang, Jin Yan Yao, Hong Zhang, Xiao Biao Shang, Han Bing Cao, Lei Yang, Gang Zhao, Wei Guo Zhang, Yong Rui, Wei Wei |
Author_xml | – sequence: 1 givenname: Ze Rui surname: Wu fullname: Wu, Ze Rui organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Department of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University – sequence: 2 givenname: Lichong surname: Yan fullname: Yan, Lichong organization: Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine – sequence: 3 givenname: Yan Ting surname: Liu fullname: Liu, Yan Ting organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Department of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University – sequence: 4 givenname: Lei surname: Cao fullname: Cao, Lei organization: Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University – sequence: 5 givenname: Yu Hang surname: Guo fullname: Guo, Yu Hang organization: Department of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University – sequence: 6 givenname: Yong surname: Zhang fullname: Zhang, Yong organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Department of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University – sequence: 7 givenname: Hong surname: Yao fullname: Yao, Hong organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 8 givenname: Lin surname: Cai fullname: Cai, Lin organization: Department of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University – sequence: 9 givenname: Han Bing surname: Shang fullname: Shang, Han Bing organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 10 givenname: Wei Wei surname: Rui fullname: Rui, Wei Wei organization: Department of Pathology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 11 givenname: Gang surname: Yang fullname: Yang, Gang organization: Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University – sequence: 12 givenname: Xiao Biao surname: Zhang fullname: Zhang, Xiao Biao organization: Department of Neurosurgery, Zhongshan Hospital, Fudan University – sequence: 13 givenname: Hao surname: Tang fullname: Tang, Hao organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 14 givenname: Yu surname: Wang fullname: Wang, Yu organization: Department of Neurosurgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 15 givenname: Jin Yan orcidid: 0000-0002-8053-0209 surname: Huang fullname: Huang, Jin Yan organization: State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 16 givenname: Yong Xu surname: Wei fullname: Wei, Yong Xu organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 17 givenname: Wei Guo surname: Zhao fullname: Zhao, Wei Guo organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 18 givenname: Bing surname: Su fullname: Su, Bing email: bingsu@sjtu.edu.cn organization: Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine – sequence: 19 givenname: Zhe Bao orcidid: 0000-0002-1611-8228 surname: Wu fullname: Wu, Zhe Bao email: zhebaowu@aliyun.com organization: Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Department of Neurosurgery, First Affiliated Hospital of Wenzhou Medical University |
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Snippet | Aberrant expression of long noncoding RNA H19 has been associated with tumour progression, but the underlying molecular tumourigenesis mechanisms remain... Abstract Aberrant expression of long noncoding RNA H19 has been associated with tumour progression, but the underlying molecular tumourigenesis mechanisms... LncRNA H19 has been shown to be aberrantly expressed in different cancers. Here, the authors show that H19 lncRNA is downregulated in pituitary adenomas and... |
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SubjectTerms | 13/89 38/109 45/61 49/88 631/337/384/2568 631/67/1459/1740 631/80/83/2359 64/86 82/51 96/1 96/31 Adaptor Proteins, Signal Transducing - metabolism Animals Brain cancer Brain tumors Cabergoline - pharmacology Carcinogenesis Carrier Proteins Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Disease Progression Disruption Down-Regulation Female Gene expression HEK293 Cells Heterografts Humanities and Social Sciences Humans Mechanistic Target of Rapamycin Complex 1 - drug effects Mechanistic Target of Rapamycin Complex 2 - metabolism Mice multidisciplinary Phosphoproteins - metabolism Phosphorylation Phosphorylation - drug effects Pituitary Pituitary gland Pituitary Neoplasms - drug therapy Pituitary Neoplasms - metabolism Ribonucleic acid Ribosomal Protein S6 Kinases, 70-kDa - metabolism RNA RNA, Long Noncoding - antagonists & inhibitors RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Science Science (multidisciplinary) Therapeutic applications TOR protein Tumorigenesis Tumors Up-Regulation |
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Title | Inhibition of mTORC1 by lncRNA H19 via disrupting 4E-BP1/Raptor interaction in pituitary tumours |
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