Evidence map›Paper›PMID 28182000›Full record

ArticleCell death & disease2017

Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth.

Xing Bao, Tingting Ren, Yi Huang, Kunkun Sun, Shidong Wang, Kuisheng Liu, Bingxin Zheng, Wei Guo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 114 citations in OpenAlex.

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  17. LncRNA-mediated DNA methylation: an emerging mechanism in cancer and beyond.Journal of experimental & clinical cancer research : CR · 2022
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1 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

8 authors at 3 institutions in 1 country.

Xing BaoMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, People's Republic of China.
Tingting RenMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, People's Republic of China.
Yi HuangMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, People's Republic of China.
Kunkun SunMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, People's Republic of China.
Shidong WangMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, People's Republic of China.
Kuisheng LiuMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, People's Republic of China.
Bingxin ZhengMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, People's Republic of China.
Wei GuoMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing, People's Republic of China.
Beijing Chest Hospital · CNPeking University · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current practices for the therapy of chondrosarcoma, including wide-margin surgical resection and chemotherapy, are less than satisfactory. Recently, emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) have an essential role in the initiation and progression of tumors. As a typical lncRNA, HOTAIR is significantly overexpressed in various tumors. However, the function and potential biological mechanisms of HOTAIR in human chondrosarcoma remain unknown. Quantitative RT-PCR demonstrated that HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. High HOTAIR expression is correlated with tumor stage and poor prognosis. Functional experiments reveal that HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo. In addition to cycle arrest and apoptosis, knockdown of HOTAIR inhibits autophagy, which favors cell death. Mechanistically, we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions, which markedly silences miR-454-3p expression. Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p, initiate HOTAIR deficiency-induced apoptosis and reduce autophagy. Collectively, our data reveal the roles and functional mechanisms of HOTAIR in human chondrosarcoma and suggest that HOTAIR may act as a prognostic biomarker and potential therapeutic target for chondrosarcoma.

Indexed as

AdolescentAnimalsApoptosisAutophagy-Related Protein 12Bone NeoplasmsCell LineCell Line, TumorCell MovementCell ProliferationChondrosarcomaDNA MethylationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMaleATG12 protein, humanAutophagy-Related Protein 12MicroRNAsMIRN454 microRNA, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID28182000
PMCPMC5386479
OpenAlexW2587513172

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.