Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a
Glioma is one of the most common and aggressive primary malignant tumor in the brain. Accumulating evidences indicated that aberrantly expressed non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), contribute to tumorigenesis. However, potential mechanisms betwe...
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| Veröffentlicht in: | Journal of experimental & clinical cancer research 2016-06, Vol.35 (1), p.90-90, Article 90 |
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| creator | Ma, Chun-Chun Xiong, Zhang Zhu, Guan-Nan Wang, Chao Zong, Gang Wang, Hong-Liang Bian, Er-Bao Zhao, Bing |
| description | Glioma is one of the most common and aggressive primary malignant tumor in the brain. Accumulating evidences indicated that aberrantly expressed non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), contribute to tumorigenesis. However, potential mechanisms between lncRNAs and miRNAs in glioma remain largely unknown.
Long non-coding RNA activated by TGF-β (LncRNA-ATB) expression in glioma tissues and cells was quantified by quantitative reverse transcription-PCR. Glioma cell lines U251 and A172 were transfected with sh-ATB, miR-200a mimics, miR-200a inhibitors, after we assayed the cell phenotype and expression of the relevant molecules. Dual-luciferase reporter assay, RIP and a xenograft mouse model were used to examine the expression of sh-ATB and its target gene miR-200a.
ATB is abnormally up-regulated both in glioma tissues and cell lines compared with normal brain tissues, and glioma patients with high ATB expression had shorter overall survival time. Knockdown of ATB significantly inhibits glioma malignancy, including cell proliferation, colony formation, migration, invasion in vitro, and the xenograft tumor formation in vivo. In addition, ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-β2.
Our findings suggest that ATB plays an oncogenic role of glioma cells by inhibiting miR-200a and facilitating TGF-β2 in glioma, thereby may represent a potential therapeutic target for the treatment of human glioma. |
| doi_str_mv | 10.1186/s13046-016-0367-2 |
| format | Article |
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Long non-coding RNA activated by TGF-β (LncRNA-ATB) expression in glioma tissues and cells was quantified by quantitative reverse transcription-PCR. Glioma cell lines U251 and A172 were transfected with sh-ATB, miR-200a mimics, miR-200a inhibitors, after we assayed the cell phenotype and expression of the relevant molecules. Dual-luciferase reporter assay, RIP and a xenograft mouse model were used to examine the expression of sh-ATB and its target gene miR-200a.
ATB is abnormally up-regulated both in glioma tissues and cell lines compared with normal brain tissues, and glioma patients with high ATB expression had shorter overall survival time. Knockdown of ATB significantly inhibits glioma malignancy, including cell proliferation, colony formation, migration, invasion in vitro, and the xenograft tumor formation in vivo. In addition, ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-β2.
Our findings suggest that ATB plays an oncogenic role of glioma cells by inhibiting miR-200a and facilitating TGF-β2 in glioma, thereby may represent a potential therapeutic target for the treatment of human glioma.</description><identifier>ISSN: 1756-9966</identifier><identifier>ISSN: 0392-9078</identifier><identifier>EISSN: 1756-9966</identifier><identifier>DOI: 10.1186/s13046-016-0367-2</identifier><identifier>PMID: 27267902</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adolescent ; Adult ; Aged ; Animals ; Brain Neoplasms - genetics ; Brain Neoplasms - pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Complications and side effects ; Female ; Gene Expression Regulation, Neoplastic ; Glioma - genetics ; Glioma - pathology ; Gliomas ; Humans ; Influence ; Male ; Mice ; MicroRNA ; MicroRNAs - genetics ; Middle Aged ; Neoplasm Invasiveness ; Neoplasm Transplantation ; Prognosis ; RNA, Long Noncoding - genetics ; Transforming Growth Factor beta2 - genetics ; Transforming growth factors ; Up-Regulation ; Young Adult</subject><ispartof>Journal of experimental & clinical cancer research, 2016-06, Vol.35 (1), p.90-90, Article 90</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>The Author(s). 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-7c80e34e01ff2b7b48ba58f0255868a5ebe9100ae1fab4074cf906ec867054b3</citedby><cites>FETCH-LOGICAL-c525t-7c80e34e01ff2b7b48ba58f0255868a5ebe9100ae1fab4074cf906ec867054b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4895888/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4895888/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27267902$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Chun-Chun</creatorcontrib><creatorcontrib>Xiong, Zhang</creatorcontrib><creatorcontrib>Zhu, Guan-Nan</creatorcontrib><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Zong, Gang</creatorcontrib><creatorcontrib>Wang, Hong-Liang</creatorcontrib><creatorcontrib>Bian, Er-Bao</creatorcontrib><creatorcontrib>Zhao, Bing</creatorcontrib><title>Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a</title><title>Journal of experimental & clinical cancer research</title><addtitle>J Exp Clin Cancer Res</addtitle><description>Glioma is one of the most common and aggressive primary malignant tumor in the brain. Accumulating evidences indicated that aberrantly expressed non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), contribute to tumorigenesis. However, potential mechanisms between lncRNAs and miRNAs in glioma remain largely unknown.
Long non-coding RNA activated by TGF-β (LncRNA-ATB) expression in glioma tissues and cells was quantified by quantitative reverse transcription-PCR. Glioma cell lines U251 and A172 were transfected with sh-ATB, miR-200a mimics, miR-200a inhibitors, after we assayed the cell phenotype and expression of the relevant molecules. Dual-luciferase reporter assay, RIP and a xenograft mouse model were used to examine the expression of sh-ATB and its target gene miR-200a.
ATB is abnormally up-regulated both in glioma tissues and cell lines compared with normal brain tissues, and glioma patients with high ATB expression had shorter overall survival time. Knockdown of ATB significantly inhibits glioma malignancy, including cell proliferation, colony formation, migration, invasion in vitro, and the xenograft tumor formation in vivo. In addition, ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-β2.
Our findings suggest that ATB plays an oncogenic role of glioma cells by inhibiting miR-200a and facilitating TGF-β2 in glioma, thereby may represent a potential therapeutic target for the treatment of human glioma.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Complications and side effects</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>Gliomas</subject><subject>Humans</subject><subject>Influence</subject><subject>Male</subject><subject>Mice</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Transplantation</subject><subject>Prognosis</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Transforming Growth Factor beta2 - genetics</subject><subject>Transforming growth factors</subject><subject>Up-Regulation</subject><subject>Young Adult</subject><issn>1756-9966</issn><issn>0392-9078</issn><issn>1756-9966</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkl1rHCEUhqW0NGnaH9CbMlAovZlUnRk_bgrb0C9YUgh7L457nDU4utWZwP77umyS7oYg4lGf9xUPL0LvCb4kRLAvmTS4ZTUmZTaM1_QFOie8Y7WUjL08qs_Qm5xvMWZEEvkanVFOGZeYnqPVMoahCjHUJq5dKW-uF9Vi9a3apjjGCXI1eBdHXY3auyHoYHZVv6sCDHpyd-B3VYJh9mVTtKO7qSnG-i16ZbXP8O5-vUCrH99XV7_q5Z-fv68Wy9p0tJtqbgSGpgVMrKU971vR605YTLtOMKE76EGSYgfE6r7FvDVWYgZGMI67tm8u0NeD7XbuR1gbCFPSXm2TG3XaqaidOr0JbqOGeKdaITshRDH4fG-Q4t8Z8qRGlw14rwPEOSvCC8cYk6SgH5-gt3FOofxOEYEx522B_lOD9qBcsLG8a_amatGyRhDBmz11-QxVxhpGZ2IA68r5ieDTkWAD2k-bHP08uRjyKUgOoEkx5wT2sRkEq31k1CEyqkRG7SOjaNF8OO7io-IhI80_8mW5gg</recordid><startdate>20160606</startdate><enddate>20160606</enddate><creator>Ma, Chun-Chun</creator><creator>Xiong, Zhang</creator><creator>Zhu, Guan-Nan</creator><creator>Wang, Chao</creator><creator>Zong, Gang</creator><creator>Wang, Hong-Liang</creator><creator>Bian, Er-Bao</creator><creator>Zhao, Bing</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160606</creationdate><title>Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a</title><author>Ma, Chun-Chun ; 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Accumulating evidences indicated that aberrantly expressed non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), contribute to tumorigenesis. However, potential mechanisms between lncRNAs and miRNAs in glioma remain largely unknown.
Long non-coding RNA activated by TGF-β (LncRNA-ATB) expression in glioma tissues and cells was quantified by quantitative reverse transcription-PCR. Glioma cell lines U251 and A172 were transfected with sh-ATB, miR-200a mimics, miR-200a inhibitors, after we assayed the cell phenotype and expression of the relevant molecules. Dual-luciferase reporter assay, RIP and a xenograft mouse model were used to examine the expression of sh-ATB and its target gene miR-200a.
ATB is abnormally up-regulated both in glioma tissues and cell lines compared with normal brain tissues, and glioma patients with high ATB expression had shorter overall survival time. Knockdown of ATB significantly inhibits glioma malignancy, including cell proliferation, colony formation, migration, invasion in vitro, and the xenograft tumor formation in vivo. In addition, ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-β2.
Our findings suggest that ATB plays an oncogenic role of glioma cells by inhibiting miR-200a and facilitating TGF-β2 in glioma, thereby may represent a potential therapeutic target for the treatment of human glioma.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27267902</pmid><doi>10.1186/s13046-016-0367-2</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Adult Aged Animals Brain Neoplasms - genetics Brain Neoplasms - pathology Cell Line, Tumor Cell Movement Cell Proliferation Complications and side effects Female Gene Expression Regulation, Neoplastic Glioma - genetics Glioma - pathology Gliomas Humans Influence Male Mice MicroRNA MicroRNAs - genetics Middle Aged Neoplasm Invasiveness Neoplasm Transplantation Prognosis RNA, Long Noncoding - genetics Transforming Growth Factor beta2 - genetics Transforming growth factors Up-Regulation Young Adult |
| title | Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a |
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