Evidence map›Paper›PMID 34729252›Full record

ArticleMolecular therapy. Nucleic acids2021

Suppression of endothelial miR-22 mediates non-small cell lung cancer cell-induced angiogenesis.

Yuan Gu, Gianni Pais, Vivien Becker, Christina Körbel, Emmanuel Ampofo, Elke Ebert, Johannes Hohneck, Nicole Ludwig, Eckart Meese, Rainer M Bohle and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.8field-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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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  3. Nodular fasciitis of the intradural cervical spine with *MIR22HG::USP6* fusion a rare postoperative occurrence and novel molecular pathogenesis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
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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

13 authors at 2 institutions in 2 countries.

Yuan GuInstitute for Clinical and Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany.
Gianni PaisInstitute for Clinical and Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany.
Vivien BeckerInstitute for Clinical and Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany.
Christina KörbelInstitute for Clinical and Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany.
Emmanuel AmpofoInstitute for Clinical and Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany.
Elke EbertInstitute of Pathology, Saarland University, 66421 Homburg/Saar, Germany.
Johannes HohneckInstitute of Pathology, Saarland University, 66421 Homburg/Saar, Germany.
Nicole LudwigInstitute of Human Genetics, Saarland University, 66421 Homburg/Saar, Germany.
Eckart MeeseInstitute of Human Genetics, Saarland University, 66421 Homburg/Saar, Germany.
Rainer M BohleInstitute of Pathology, Saarland University, 66421 Homburg/Saar, Germany.
Yingjun ZhaoFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Michael D MengerInstitute for Clinical and Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany.
Matthias W LaschkeInstitute for Clinical and Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany.
Saarland University · DEFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) expressed in endothelial cells (ECs) are powerful regulators of angiogenesis, which is essential for tumor growth and metastasis. Here, we demonstrated that miR-22 is preferentially and highly expressed in ECs, while its endothelial level is significantly downregulated in human non-small cell lung cancer (NSCLC) tissues when compared to matched nontumor lung tissues. This reduction of endothelial miR-22 is possibly induced by NSCLC cell-secreted interleukin-1β and subsequently activated transcription factor nuclear factor-κB. Endothelial miR-22 functions as a potent angiogenesis inhibitor that inhibits all of the key angiogenic activities of ECs and consequently NSCLC growth through directly targeting sirtuin 1 and fibroblast growth factor receptor 1 in ECs, leading to inactivation of AKT/mammalian target of rapamycin signaling. These findings provide insight into the molecular mechanisms of NSCLC angiogenesis and indicate that endothelial miR-22 represents a potential target for the future antiangiogenic treatment of NSCLC.

Indexed as

AKTangiogenesisendothelial cellsFGFR1IL-1βmiR-22NF-κBNSCLCSIRT1vascularization

Identifiers

PMID34729252
PMCPMC8536510
OpenAlexW3205158811

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.