Evidence map›Paper›PMID 38162062›Full record

ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2023

[Preliminary Investigation of the Molecular Mechanism of Empagliflozin Suppressing Gastric Cancer Through Mammalian Target of Rapamycin].

Huiling Rao, Wang Cheng, Juan Yu, Xiaotong An, Haojun Deng, Zhaoyang Zhang, Fuyun Wu, Fuyun Ji, Shan Li

Open access · greenAbstract readEnglish Abstract
In one paragraph

Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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 1 institution in 1 country.

Huiling Rao( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Wang Cheng( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Juan Yu( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Xiaotong An( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Haojun Deng( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Zhaoyang Zhang( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Fuyun Wu( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Fuyun Ji( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Shan Li( 442000) Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China.
Hubei University of Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To predict the intervention targets of empagliflozin (EMPA), a specific inhibitor of sodium-glucose cotransporter 2 (SGLT2), in gastric adenocarcinoma through comprehensive network pharmacology, and to validate the effects and the molecular mechanisms of EMPA through cellular and molecular biology experiments. Methods: Bioinformatics analysis of gastric adenocarcinoma was conducted to assess the correlation between gastric adenocarcinoma prognosis and SGLT2 expression. Network pharmacology was utilized to identify shared targets of EMPA and gastric adenocarcinoma. AGS cells, a human gastric adenocarcinoma cells line, were incubated with EMPA at different concentrations for 24 h and, then, cell proliferation was assessed using the CCK8 assay. After AGS cells were incubated with EMPA at the doses of 0, 3, and 6 mmol/L, real-time cell analysis (RTCA) and 5-ethynyl-2-deoxyuridine (EdU) incorporation were used to evaluate EMPA's inhibitory effects on the proliferation of the AGS cells. In addition, wound healing and Transwell assays were performed to assess the inhibitory effect of EMPA on the migration and invasion of the APC cells and Western blot analysis was conducted to examine the expression of mammalian target of rapamycin (mTOR) and phosphorylated mTOR (p-mTOR). BALB/c (nu/nu) nude mice were implanted with 5×10 Results: Gastric adenocarcinoma patients with low expression of SGLT2 exhibited longer survival time and higher survival rate than those with high expression of SGLT2 did. A total of 104 EMPA-related potential targets and 2028 targets associated with gastric adenocarcinoma were identified. Among these, 45 targets associated with gastric adenocarcinoma overlapped with potential targets of EMPA. Further analysis revealed 10 relevant pathways and 4 core genes. The core genes were cyclin-dependent kinase 4 ( Conclusion: EMPA inhibits the abnormal proliferation and migration of gastric adenocarcinoma cells, potentially through the modulation of mTOR protein activation. This study provides new potential medication and intervention targets for gastric adenocarcinoma treatment.

Indexed as

AdenocarcinomaSodium-Glucose Transporter 2 InhibitorsStomach NeoplasmsTOR Serine-Threonine KinasesAnimalsBenzhydryl CompoundsCell Line, TumorCell ProliferationGlucosidesHumansMiceMice, NudeSignal TransductionSirolimusSodium-Glucose Transporter 2Benzhydryl CompoundsempagliflozinGlucosidesSirolimusSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsTOR Serine-Threonine KinasesEmpagliflozinGastric adenocarcinomaIntegrated network pharmacologymTORSodium-glucose cotransporter 2

Identifiers

PMID38162062
PMCPMC10752783
OpenAlexW4390508061

What OpenQuestion 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 OpenQuestion graph.