Evidence map›Paper›PMID 27811366›Full record

ArticleOncotarget2016

MiR-21 and MiR-155 promote non-small cell lung cancer progression by downregulating SOCS1, SOCS6, and PTEN.

Xinying Xue, Yuxia Liu, Yong Wang, Mingming Meng, Kaifei Wang, Xuefeng Zang, Sheng Zhao, Xiaohua Sun, Lei Cui, Lei Pan and 1 more

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

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 3 pooled it
7.7field-weighted citation impact, top 2% 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

110 citing papers in PubMed, 3 syntheses or guidelines pooled it, 181 citations in OpenAlex.

  1. Pooled it
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  8. Review
  9. microRNA-155: a versatile noncoding RNA.Molecular biology reports · 2026
    Review
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50 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

11 authors at 7 institutions in 1 country.

Xinying XueDepartment of Special Medical Treatment-Respiratory Disease, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Yuxia LiuDepartment of Research, Peking Union Medical Collage Hospital, Beijing, China.
Yong WangDepartment of Special Medical Treatment-Respiratory Disease, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Mingming MengDepartment of Gastroenterology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Kaifei WangDepartment of Respiratory Diseases of Chinese PLA General Hospital, Beijing, China.
Xuefeng ZangDepartment of Intensive Care Unit, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Sheng ZhaoDepartment of Cardiology, Peking University Ninth School of Clinical Medicine, Beijing Shijitan Hospital, Beijing, China.
Xiaohua SunInstitute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lei CuiDepartment of Central Laboratory, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Lei PanDepartment of Special Medical Treatment-Respiratory Disease, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Sanhong LiuShanghai Institute of Advanced Immunochemical Studies, ShanghaiTech University, Shanghai, China.
Beijing Shijitan Hospital · CNCapital Medical University · CNChinese Academy of Sciences · CNChinese PLA General Hospital · CNPeking Union Medical College Hospital · CNPeking University · CNShanghaiTech University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer remains the leading cause of cancer-associated death worldwide. MiR-21 and miR-155 are the most amplified miRNAs in non-small cell lung carcinoma (NSCLC), and are critical promoters of NSCLC progression. However, it remains unclear how miR-21 and miR-155 induce cancer progression, and whether these miRNAs share common targets, such as tumor suppressor genes required to prevent NSCLC. Here we report that miR-21 and miR-155 levels are elevated in NSCLC and are proportional to the progression of the disease. In addition, miR-21 and miR-155 share nearly 30% of their predicted target genes, including SOCS1, SOCS6, and PTEN, three tumor suppressor genes often silenced in NSCLC. Consequently, antagonizing miR-21, miR-155 or both potently inhibited tumor progression in xenografted animal models of NSCLC. Treatment with miR-21 and miR-155 inhibitors in combination was always more effective against NSCLC than treatment with a single inhibitor. Furthermore, levels of miR-21 and miR-155 expression correlated inversely with overall and disease-free survival of NSCLC patients. Our findings reveal that miR-21 and miR-155 promote the development of NSCLC, in part by downregulating SOCS1, SOCS6, and PTEN. Combined inhibition of miR-21 and miR-155 could improve the treatment of NSCLC.

Indexed as

Gene Expression Regulation, NeoplasticA549 CellsAnimalsAntagomirsCarcinoma, Non-Small-Cell LungCell Line, TumorDisease-Free SurvivalDisease ProgressionDown-RegulationHumansLung NeoplasmsMaleMice, Inbred BALB CMice, NudeMicroRNAsPTEN PhosphohydrolaseAntagomirsMicroRNAsMIRN155 microRNA, humanMIRN21 microRNA, humanPTEN PhosphohydrolaseSOCS1 protein, humanSOCS6 protein, humanSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTumor Suppressor ProteinsmiR-155miR-21non-small cell lung carcinomaSOCS1SOCS6

Identifiers

PMID27811366
PMCPMC5356677
OpenAlexW2548791365

What OpenQuestion holds

Textmetadata
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.