Evidence map›Paper›PMID 32855383›Full record

ArticleCell death & disease2020

PGAM1, regulated by miR-3614-5p, functions as an oncogene by activating transforming growth factor-β (TGF-β) signaling in the progression of non-small cell lung carcinoma.

Fangfang Li, Hao Yang, Tiandong Kong, Shanshan Chen, Ping Li, Lu Chen, Jiuling Cheng, Guangying Cui, Guojun Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Fangfang Li *Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Hao Yang *Department of Orthopedics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Tiandong Kong *Department of Oncology, The Third People's Hospital of Zhengzhou, Zhengzhou, 450000, China.
Shanshan ChenDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Ping LiDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Lu ChenDepartment of Oncology, The Third People's Hospital of Zhengzhou, Zhengzhou, 450000, China.
Jiuling ChengDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Guangying CuiPrecision Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. cuiguangying1986@163.com.
Guojun ZhangDepartment of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. gjzhangzzu@126.com.
First Affiliated Hospital of Zhengzhou University · CNZhengzhou People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphoglycerate mutase 1 (PGAM1) is a recently identified key catalytic enzyme in aerobic glycolysis. Recent literature has documented that dysregulated PGAM1 expression is associated with tumorigenesis in various cancers. However, the expression status and biological function of PGAM1 in non-small-cell lung cancer (NSCLC) are poorly elucidated. In this study, we found that PGAM1 was overexpressed in NSCLC tissues and that high expression of PGAM1 was associated with poor prognosis in NSCLC patients. Functionally, gain- and loss-of-function analysis showed that PGAM1 promoted proliferation and invasion in vitro, and facilitated tumor growth in vivo. Mechanistically, the transforming growth factor-β (TGF-β) signaling pathway was also markedly impaired in response to PGAM1 silencing. Additionally, we verified that PGAM1 was inhibited by miR-3614-5p via direct targeting of its 3'-untranslated regions in a hypoxia-independent manner. Furthermore, overexpression of miR-3614-5p attenuated NSCLC cell proliferation and invasion, and these effects could be partially reversed by reintroduction of PGAM1. Conclusively, our results suggest that the miR-3614-5p/PGAM1 axis plays a critical role during the progression of NSCLC, and these findings may provide a potential target for the development of therapeutic strategies for NSCLC patients.

Indexed as

AdultAgedCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationChinaDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMicroRNAsMiddle AgedmicroRNA 3614, humanMicroRNAsPhosphoglycerate Mutasephosphoglycerate mutase 1, humanTransforming Growth Factor betaTransforming Growth Factors

Identifiers

PMID32855383
PMCPMC7453026
OpenAlexW3080185518

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.