Evidence map›Paper›PMID 34461940›Full record

ArticleJournal of translational medicine2021

GSK2126458 has the potential to inhibit the proliferation of pancreatic cancer uncovered by bioinformatics analysis and pharmacological experiments.

Yueqin Feng, Yuguan Jiang, Fengjin Hao

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

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  6. Screening of Therapeutic Targets for Pancreatic Cancer by Bioinformatics Methods.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2023
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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

3 authors at 1 institution in 1 country.

Yueqin FengDepartment of Ultrasound, The First Affiliated Hospital of China Medical University, Shenyang, 110022, Liaoning, China. fengjinyueqin@163.com.
Yuguan JiangSchool of Pharmacy, China Medical University, Shenyang, 110122, Liaoning, China.
Fengjin HaoDepartment of Biochemistry and Molecular Biology, China Medical University, Shenyang, 110122, Liaoning, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic cancer is one of the most serious digestive malignancies. At present, there is an extreme lack of effective strategies in clinical treatment. The purpose of this study is to identify key genes and pathways in the development of pancreatic cancer and provide targets for the treatment of pancreatic cancer.

methodsGSE15471 and GSE62165 were used to screen differentially expressed genes by GEO2R tool. Hub genes prognostic potential assessed using the GEPIA and Kaplan-Meier plotter databases. The drug susceptibility data of pan-cancer cell lines is provided by The Genomics of Drug Sensitivity in Cancer Project (GDSC). Finally, the effects of PI3K-Akt signaling pathway inhibitors on cell viability of pancreatic cancer cells were detected by cell proliferation and invasion assays.

resultsA total of 609 differentially expressed genes were screened and enriched in the focal adhesion, phagosome and PI3K-Akt signaling pathway. Of the 15 hub genes we found, four were primarily associated with the PI3K-Akt signaling pathway, including COL3A1, EGF, FN1 and ITGA2. GDSC analysis showed that mTOR inhibitors are very sensitive to pancreatic cancer cells with mutations in EWSR1.FLI1 and RNF43. Cell proliferation and invasion results showed that mTOR inhibitors (GSK2126458) can inhibit the proliferation of pancreatic cancer cells.

conclusionsThis study suggested that the PI3K-Akt signaling pathway may be a key pathway for pancreatic cancer, our study uncovered the potential therapeutic potential of GSK2126458, a specific mTOR inhibitor, for pancreatic cancer.

Indexed as

Computational BiologyPancreatic NeoplasmsBenzenesulfonamidesCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesPyridazinesQuinolinesSulfonamidesBenzenesulfonamidesomipalisibPhosphatidylinositol 3-KinasesPyridazinesQuinolinesSulfonamidesBioinformatics analysisDAVIDGEOPancreatic cancerPI3K–Akt

Identifiers

PMID34461940
PMCPMC8406597
OpenAlexW3197408247

What OpenQuestion holds

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LicenceCC BY
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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.