Evidence map›Paper›PMID 29336659›Full record

ArticleCancer biology & therapy2018

Long non-coding RNA HOTAIR promotes cervical cancer progression through regulating BCL2 via targeting miR-143-3p.

Mingzhu Liu, Jinying Jia, Xinjie Wang, Yanjie Liu, Chunfang Wang, Ruitai Fan

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

73 citing papers in PubMed, 125 citations in OpenAlex.

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  12. Diagnostic value for methylation in cervical cancer based on a small-molecule fluorescent probe targeting DNMT1.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
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13 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Mingzhu Liua Department of Integrated Traditional Chinese and Western Medicine , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
Jinying Jiaa Department of Integrated Traditional Chinese and Western Medicine , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
Xinjie Wanga Department of Integrated Traditional Chinese and Western Medicine , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
Yanjie Liub Department of Gynecology , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
Chunfang Wangb Department of Gynecology , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
Ruitai Fanc Department of Radiotherapy , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHOX transcript antisense RNA (HOTAIR) is a long non-coding RNA (lncRNA) widely involved in the progression of numerous malignancies. Whereas, the potential molecular mechanism of HOTAIR involved in cervical cancer progression is still needed to be elaborated.

methodsThe expression of HOTAIR and miR-143-3p were detected in cervical cancer tissues and cells by qRT-PCR. MTT and flow cytometry analysis were performed to measure cell proliferation and apoptosis. Bioinformatics, Dual-Luciferase reporter and RIP were used to analyze the possible correlation between HOTAIR, miR-143-3p and BCL2. The expression of Bax and BCL2 was detected by western blot. Mice xenograft model was established to confirm the role of HOTAIR on tumor growth in vivo.

resultsHOTAIR expression was elevated while miR-143-3p expression was reduced in cervical cancer tissues and cell lines. HOTAIR knockdown suppressed proliferation and enhanced apoptosis in cervical cancer cells. Moreover, HOTAIR could function as a sponge for miR-143-3p. The inhibitory effect of HOTAIR knockdown on cervical cancer cells growth was abolished following decrease of miR-143-3p expression. Furthermore, HOTAIR promoted BCL2 expression by modulating miR-143-3p. BCL2 overexpression attenuated the tumor-suppressive effect of miR-143-3p in cervical cancer. Finally, the carcinogenicity of HOTAIR was validated in mice.

conclusionsHOTAIR promoted cervical cancer cell growth by modulating BCL2 via miR-143-3p, hinting a novel regulatory mechanism and potential therapeutic target in cervical cancer.

Indexed as

AnimalsCell Line, TumorDisease ProgressionFemaleHeLa CellsHeterograftsHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsProto-Oncogene Proteins c-bcl-2RNA, Long NoncodingTransfectionUterine Cervical NeoplasmsBCL2 protein, humanHOTAIR long untranslated RNA, humanMicroRNAsMIRN143 microRNA, humanProto-Oncogene Proteins c-bcl-2RNA, Long NoncodingBCL2cervical cancerHOTAIRlncRNAmiR-143-3p

Identifiers

PMID29336659
PMCPMC5915047
OpenAlexW2783089488

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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.