Evidence map›Paper›PMID 30900402›Full record

ArticleThoracic cancer2019

miR-194 suppresses high glucose-induced non-small cell lung cancer cell progression by targeting NFAT5.

Xuying Meng, Zhenjin Li, Saijun Zhou, Shumin Xiao, Pei Yu

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 34 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

5 authors at 1 institution in 1 country.

Xuying MengDepartment of Diabetic Nephropathy Hemodialysis, Key Laboratory of Hormone and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Disease, The Metabolic Disease Hospital of Tianjin Medical University, Tianjin, China.
Zhenjin LiDepartment of Diabetic Nephropathy Hemodialysis, Key Laboratory of Hormone and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Disease, The Metabolic Disease Hospital of Tianjin Medical University, Tianjin, China.
Saijun ZhouDepartment of Diabetic Nephropathy Hemodialysis, Key Laboratory of Hormone and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Disease, The Metabolic Disease Hospital of Tianjin Medical University, Tianjin, China.
Shumin XiaoDepartment of Diabetic Nephropathy Hemodialysis, Key Laboratory of Hormone and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Disease, The Metabolic Disease Hospital of Tianjin Medical University, Tianjin, China.
Pei YuDepartment of Diabetic Nephropathy Hemodialysis, Key Laboratory of Hormone and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Disease, The Metabolic Disease Hospital of Tianjin Medical University, Tianjin, China.ORCID 0000-0003-0313-3530
Tianjin Infectious Diseases Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes mellitus (DM) is linked to an increased risk of lung cancer; however, the exact molecular basis is unclear.

methodsWe used a microarray method and found a group of microRNAs differently expressed in lung cancer cells at high or low glucose treatment.

resultsAmong these, miR-194 changed significantly, which indicated further analysis. miR-194 was significantly downregulated in non-small cell lung cancer (NSCLC) cells cultured in high glucose (HG) medium and clinical NSCLC tissues with DM. The introduction of miR-194 significantly suppressed the proliferation, migration, and invasion of lung cancer cells induced by HG, suggesting that miR-194 may be a suppressor during HG-induced NSCLC progression. Further analysis indicated that NFAT5 was a direct target gene of miR-194, evidenced by the direct binding of miR-194 with the 3'untranslated region of NFAT5. MiR-194 could decrease the expression of NFAT5 at both messenger RNA and protein levels, while overexpression of NFAT5 reversed the decreased proliferation, migration, and invasion ability mediated by miR-194 in lung cancer cells.

conclusionOur findings provide new insight into the mechanism of NSCLC progression. Therapeutically, miR-194 may serve as a potential target for the treatment of lung cancer patients with DM.

Indexed as

Gene Expression Regulation, NeoplasticCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationCells, CulturedFemaleGlucoseHumansLung NeoplasmsMaleMicroRNAsRNA InterferenceTranscription FactorsGlucoseMicroRNAsMIRN194 microRNA, humanNFAT5 protein, humanTranscription FactorsHGLGMiR-194NFAT5NSCLC

Identifiers

PMID30900402
PMCPMC6500961
OpenAlexW2924493233

What Socratic holds

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LicenceCC BY-NC
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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 Socratic graph.