Evidence map›Paper›PMID 29391067›Full record

ArticleCell communication and signaling : CCS2018

LncRNA HOTAIR promotes cell migration and invasion by regulating MKL1 via inhibition miR206 expression in HeLa cells.

Peng Zheng, Ze Yin, Ying Wu, Yao Xu, Ying Luo, Tong-Cun Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 55 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Peng ZhengCollege of Life Science and Healthy, Wuhan University of Science and technology, Wuhan, 430065, China. pengzh1984@wust.edu.cn.ORCID 0000-0001-6595-7477
Ze YinCollege of Life Science and Healthy, Wuhan University of Science and technology, Wuhan, 430065, China.
Ying WuKey Laboratory of Algal Biology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, 430072, China.
Yao XuCollege of Life Science and Healthy, Wuhan University of Science and technology, Wuhan, 430065, China.
Ying LuoCollege of Life Science and Healthy, Wuhan University of Science and technology, Wuhan, 430065, China.
Tong-Cun ZhangCollege of Life Science and Healthy, Wuhan University of Science and technology, Wuhan, 430065, China. zhangtongcun@wust.edu.cn.
Wuhan University of Science and Technology · CNChinese Academy of Sciences · CNWuchang University of Technology · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong 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.

methodsThe 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.

resultIn 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.

conclusionThese 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.

Indexed as

3' Untranslated RegionsAntagomirsBase SequenceCell MovementFemaleHeLa CellsHumansMicroRNAsPromoter Regions, GeneticRNA InterferenceRNA, Long NoncodingRNA, Small InterferingTrans-ActivatorsUterine Cervical Neoplasms3' Untranslated RegionsAntagomirsHOTAIR long untranslated RNA, humanMicroRNAsMIRN206 microRNA, humanMRTFA protein, humanRNA, Long NoncodingRNA, Small InterferingTrans-ActivatorsHOTAIRInvasionMigrationmiR206MKL1

Identifiers

PMID29391067
PMCPMC5796349
OpenAlexW2802101645

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.