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LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells
Zheng, Peng1,2; Yin, Ze1; Wu, Ying3; Xu, Yao1,2; Luo, Ying1; Zhang, Tong-Cun1,2
Corresponding AuthorZheng, Peng(pengzh1984@wust.edu.cn) ; Zhang, Tong-Cun(zhangtongcun@wust.edu.cn)
2018-02-01
Source PublicationCELL COMMUNICATION AND SIGNALING
ISSN1478-811X
Volume16Pages:15
AbstractBackground: Long non-coding RNAs (lncRNAs) have emerged as a new and crucial layer of gene regulation in recent years and regulate various biological processes such as carcinogenesis and metastasis. LncRNA HOTAIR, an oncogenic lncRNA, is involved in human tumorigenesis and dysregulated in cervical cancer. Megakaryoblastic leukemia 1 (MKL1), as a transcription coactivity factor, involved in cancer metastasis and cell differentiation. However, the precise mechanism of biological roles of HOTAIR and MKL1 in cancer cells remain unclear. Methods: The expression levels of HOTAIR and MKL1 were measured by quantitative PCR (qPCR), immunoblotting, in situ hybridization (ISH) and immunohistochemistry (IHC). Wound-healing and transwell assays were used to examine the invasive abilities of HeLa cells. Luciferase reporter assays and CHIP were used to determine how MKL1 regulates HOTAIR. Tissue microarray and immunohistochemical staining were used to assess the correlation between HOTAIR and MKL1 in Cervical cancer tissues in vivo. Result: In this study, we have identified that MKL1 had a role in the induction of migration and invasion in cervical cancer cells. Moreover, the expression level of MKL1, as the targeting gene of miR206, was decreased after HOTAIR inhibition in HeLa cells. Agreement with it, Highly level of MKL1 correlation with HOTAIR is validated in cervical cancer tissues. Importantly, HOTAIR is observed to participate in the silencing of miR206 expression. Interestingly, HOTAIR inhibition could also accelerate the expression of MKL1 in cytoplasm. What is more, MKL1 can activate the transcription of HOTAIR through binding the CArG box in the promoter of HOTAIR. Conclusion: These elucidates that the phenotypic effects of migration and invasion observed after HOTAIR inhibition, at least in part, through the regulation of MKL1 via inhibition of miR206 expression in HeLa cells. These data indicate the existence of a positive feedback loop between HOTAIR and MKL1. Together, these findings suggest that MKL1 is an important player in the functions of HOTAIR in the migration and invasion of cancer cells.
KeywordHOTAIR MKL1 miR206 Migration Invasion
DOI10.1186/s12964-018-0216-3
Funding OrganizationNational Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province
Indexed BySCI ; SCI
Language英语
Funding ProjectNational Natural Science Foundation of China[31500622] ; program of Wuhan University of Science and technology[25011401] ; Science and technology research project of Hubei Province[B2016004]
WOS Research AreaCell Biology
WOS SubjectCell Biology
WOS IDWOS:000423817500001
WOS KeywordLONG NONCODING RNA ; SERUM RESPONSE FACTOR ; TRANSCRIPTION FACTOR ; BREAST-CANCER ; STEM-CELLS ; HEPATOCELLULAR-CARCINOMA ; COACTIVATOR MKL1 ; GENE-EXPRESSION ; X-CHROMOSOME ; FACTOR SRF
PublisherBIOMED CENTRAL LTD
Funding OrganizationNational Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; program of Wuhan University of Science and technology ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province ; Science and technology research project of Hubei Province
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Cited Times:12[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/342005/29976
Collection其他_期刊论文
Corresponding AuthorZheng, Peng; Zhang, Tong-Cun
Affiliation1.Wuhan Univ Sci & Technol, Coll Life Sci & Hlth, Wuhan 430065, Hubei, Peoples R China
2.Wuhan Univ Sci & Technol, Inst Biol & Med, Wuhan 430065, Hubei, Peoples R China
3.Chinese Acad Sci, Inst Hydrobiol, Key Lab Algal Biol, Wuhan 430072, Hubei, Peoples R China
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GB/T 7714
Zheng, Peng,Yin, Ze,Wu, Ying,et al. LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells[J]. CELL COMMUNICATION AND SIGNALING,2018,16:15.
APA Zheng, Peng,Yin, Ze,Wu, Ying,Xu, Yao,Luo, Ying,&Zhang, Tong-Cun.(2018).LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells.CELL COMMUNICATION AND SIGNALING,16,15.
MLA Zheng, Peng,et al."LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells".CELL COMMUNICATION AND SIGNALING 16(2018):15.
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