The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer
Recently, the long non-coding RNA (lncRNA) H19 has been identified as an oncogenic gene in multiple cancer types and elevated expression of H19 was tightly linked to tumorigenesis and cancer progression. However, the molecular basis for this observation has not been characterized in colorectal cance...
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| Published in | Oncotarget Vol. 6; no. 26; pp. 22513 - 22525 |
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| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Impact Journals LLC
08.09.2015
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Recently, the long non-coding RNA (lncRNA) H19 has been identified as an oncogenic gene in multiple cancer types and elevated expression of H19 was tightly linked to tumorigenesis and cancer progression. However, the molecular basis for this observation has not been characterized in colorectal cancer (CRC) especially during epithelial to mesenchymal transition (EMT) progression. In our studies, H19 was characterized as a novel regulator of EMT in CRC. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression. |
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| AbstractList | Recently, the long non-coding RNA (lncRNA) H19 has been identified as an oncogenic gene in multiple cancer types and elevated expression of H19 was tightly linked to tumorigenesis and cancer progression. However, the molecular basis for this observation has not been characterized in colorectal cancer (CRC) especially during epithelial to mesenchymal transition (EMT) progression. In our studies, H19 was characterized as a novel regulator of EMT in CRC. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression. Recently, the long non-coding RNA (lncRNA) H19 has been identified as an oncogenic gene in multiple cancer types and elevated expression of H19 was tightly linked to tumorigenesis and cancer progression. However, the molecular basis for this observation has not been characterized in colorectal cancer (CRC) especially during epithelial to mesenchymal transition (EMT) progression. In our studies, H19 was characterized as a novel regulator of EMT in CRC. We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression. |
| Author | Wong, Cheuk-Wa Xiao, Li-Jia Waye, Mary Miu-Yee Fu, Wei-Ming Wang, Wei-Mao Zhang, Li Wan, David Chi-Cheong Liang, Wei-Cheng Zhang, Jin-Fang Wang, Yan Hu, Guo-Xin |
| AuthorAffiliation | 1 School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China 2 Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China 3 Guangzhou Institute of Advanced Technology, Chinese Academy of Sciences, Guangzhou, P.R. China 5 Department of Clinical Laboratory, Nanshan Affiliated Hospital of Guangdong Medical College, Shenzhen, P.R. China 4 Department of Infectious Diseases, Peking University Shenzhen Hospital, Shenzhen, P.R. China 6 Department of Orthopaedics & Traumatology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong, P.R. China |
| AuthorAffiliation_xml | – name: 2 Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China – name: 6 Department of Orthopaedics & Traumatology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong, P.R. China – name: 1 School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China – name: 5 Department of Clinical Laboratory, Nanshan Affiliated Hospital of Guangdong Medical College, Shenzhen, P.R. China – name: 3 Guangzhou Institute of Advanced Technology, Chinese Academy of Sciences, Guangzhou, P.R. China – name: 4 Department of Infectious Diseases, Peking University Shenzhen Hospital, Shenzhen, P.R. China |
| Author_xml | – sequence: 1 givenname: Wei-Cheng surname: Liang fullname: Liang, Wei-Cheng organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China, Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China – sequence: 2 givenname: Wei-Ming surname: Fu fullname: Fu, Wei-Ming organization: Guangzhou Institute of Advanced Technology, Chinese Academy of Sciences, Guangzhou, P.R. China – sequence: 3 givenname: Cheuk-Wa surname: Wong fullname: Wong, Cheuk-Wa organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China, Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China – sequence: 4 givenname: Yan surname: Wang fullname: Wang, Yan organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China – sequence: 5 givenname: Wei-Mao surname: Wang fullname: Wang, Wei-Mao organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China – sequence: 6 givenname: Guo-Xin surname: Hu fullname: Hu, Guo-Xin organization: Department of Infectious Diseases, Peking University Shenzhen Hospital, Shenzhen, P.R. China – sequence: 7 givenname: Li surname: Zhang fullname: Zhang, Li organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China – sequence: 8 givenname: Li-Jia surname: Xiao fullname: Xiao, Li-Jia organization: Department of Clinical Laboratory, Nanshan Affiliated Hospital of Guangdong Medical College, Shenzhen, P.R. China – sequence: 9 givenname: David Chi-Cheong surname: Wan fullname: Wan, David Chi-Cheong organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China – sequence: 10 givenname: Jin-Fang surname: Zhang fullname: Zhang, Jin-Fang organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China, Department of Orthopaedics & Traumatology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong, P.R. China – sequence: 11 givenname: Mary Miu-Yee surname: Waye fullname: Waye, Mary Miu-Yee organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China, Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26068968$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Epithelial-Mesenchymal Transition - genetics HCT116 Cells HEK293 Cells Heterografts HT29 Cells Humans Mice Mice, Nude MicroRNAs - genetics MicroRNAs - metabolism Research Paper RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Up-Regulation |
| Title | The lncRNA H19 promotes epithelial to mesenchymal transition by functioning as miRNA sponges in colorectal cancer |
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