Evidence map›Paper›PMID 27857021›Full record

ArticleCancer research and treatment2017

Effects and Mechanisms of Metformin on the Proliferation of Esophageal Cancer Cells

Jian-Cai Tang, Rui An, Yi-Qing Jiang, Jian Yang

Open access · diamondAbstract read
In one paragraph

Article in Cancer research and treatment, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

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  9. Cancers · 2024
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  13. Review
  14. Review
  15. Review
  16. Article
  17. 12-Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  18. Article
  19. Review
  20. Article
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

4 authors at 1 institution in 1 country.

Jian-Cai TangDepartment of Biochemistry, North of Sichuan Medical University, Nanchong, China.
Rui AnSchool of Basic Medical Sciences, North of Sichuan Medical University, Nanchong, China.
Yi-Qing JiangSchool of Basic Medical Sciences, North of Sichuan Medical University, Nanchong, China.
Jian YangPathogenic Biology and Immunology Experiment Teaching Center, North of Sichuan Medical University, Nanchong, China.
North Sichuan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe purpose of this study was to observe the effects of metformin on human esophageal cancer cell and to investigate its possible mechanisms. MATERIALS AND

methodsCell viability was detected by using a Cell Counting Kit-8, while cell cycle and apoptosis were assessed by flow cytometry and western blot was used to measure the expression of the related proteins. RNAi was used to knockout pyruvate kinase muscle isozyme 2 (PKM2). An Eca109 tumor model was established to evaluate the antitumor effect

resultsEsophageal cancer cells viability was reduced after metformin treatment. The cell cycle was arrested in the G0/G1 phase, apoptosis was induced, caspase 3 was activated, caspase 9 was downregulated, and the pro-apoptotic protein Bim increased. Further study revealed that metformin could suppress the expression of insulin-like growth factor 1 receptor and its downstream proteins, phosphoinositide 3-kinase (PI3K), protein kinase B (AKT/PKB), phosphorylation of AKT (pAKT), mammalian target of rapamycin (mTOR), p70S6K, and PKM2. Insulin-like growth factor 1 partly reversed metfromin-induced apoptosis and attenuated the repression effect of metfomin to PI3K, pAKT, and PKM2. Knockout PKM2 resulted in the activation of caspase 3, down-regulation of caspase 9, and increased expression of Bim. In the Eca109 xenograft model, metformin significantly reduced tumor growth. Furthermore, we found that metformin treatment increased the rate of apoptosis, down-regulation of PKM2, and up-regulation of Bim in tumor tissues.

conclusionMetformin restrained esophageal cancer cell proliferation partly by suppressing the PI3K/AKT/mTOR pathway.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarrier ProteinsCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalEsophageal NeoplasmsHumansImmunohistochemistryMembrane ProteinsMetforminMicePhosphatidylinositol 3-KinasesAntineoplastic AgentsCarrier ProteinsMembrane ProteinsMetforminPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSomatomedinsThyroid Hormone-Binding ProteinsThyroid HormonesTOR Serine-Threonine KinasesApoptosisBcl-2-interacting mediator of cell deathCell proliferationMetforminPKM2 protein

Identifiers

PMID27857021
PMCPMC5512357
OpenAlexW2557083980

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.