Evidence map›Paper›PMID 29029436›Full record

ArticleOncotarget2017

XIST/miR-139 axis regulates bleomycin (BLM)-induced extracellular matrix (ECM) and pulmonary fibrosis through β-catenin.

Yichun Wang, Ying Liang, Junming Luo, Jing Nie, Huiming Yin, Qiong Chen, Jing Dong, Jixiang Zhu, Jiamei Xia, Wei Shuai

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. FASEB bioAdvances · 2026
    Article
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  10. Biological Function of Long Non-coding RNA (LncRNA) Xist.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Article
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  15. Review
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

10 authors at 2 institutions in 1 country.

Yichun WangCritical Care Medicine Department, Hunan Cancer Hospital, Changsha, China.
Ying LiangDepartment of Food Science and Engineering, Central South University of Forestry and Technology, Changsha, China.
Junming LuoCritical Care Medicine Department, Hunan Cancer Hospital, Changsha, China.
Jing NieCritical Care Medicine Department, Hunan Cancer Hospital, Changsha, China.
Huiming YinRespiratory Medicine Department, The First Affiliated Hospital of Hunan University of Medicine, Changsha, China.
Qiong ChenCritical Care Medicine Department, Hunan Cancer Hospital, Changsha, China.
Jing DongCritical Care Medicine Department, Hunan Cancer Hospital, Changsha, China.
Jixiang ZhuCritical Care Medicine Department, Hunan Cancer Hospital, Changsha, China.
Jiamei XiaCritical Care Medicine Department, Hunan Cancer Hospital, Changsha, China.
Wei ShuaiCritical Care Medicine Department, Hunan Cancer Hospital, Changsha, China.
Hunan Cancer Hospital · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis (PF), characterized by the destruction of lung tissue architecture and the abnormal deposition of extracellular matrix (ECM) proteins, currently has no satisfactory treatment. In the present study, we investigated the hypothesis that XIST play a promotive role in bleomycin (BLM)-induced ECM and pulmonary fibrosis; XIST exerts its effect through miR-139 regulation. XIST expression was upregulated in lung tissues derived from BLM-induced mouse model of PF, and was positively correlated with β-catenin and ECM protein levels, respectively. LV-sh-XIST-induced XIST knockdown led to decreased PF, reduced β-catenin and ECM protein levels in lung tissues. XIST knockdown suppressed the proliferation of IMR-90 (human fibroblast) and murine lung fibroblasts (MLFCs) and ECM protein expression. Moreover, miR-139 could directly bind to XIST and the 3'UTR of β-catenin; XIST competed with β-catenin for miR-139 binding both in IMR-90 and MLFCs. In MLFCs, miR-139 inversely regulated XIST, and could partially reverse the effect of XIST on β-catenin and ECM proteins. In lung tissues of PF mice, miR-139 expression was downregulated, whereas β-catenin expression was upregulated. In conclusion, XIST exerts positive effects on BLM-induced PF through inhibiting miR-139 to promote human/mouse fibroblast proliferation and ECM proteins.

Indexed as

extracellular matrix (ECM)fibroblastpulmonary fibrosis (PF)XIST/miR-139β-catenin

Identifiers

PMID29029436
PMCPMC5630336
OpenAlexW2619242555

What OpenQuestion holds

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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.