Evidence map›Paper›PMID 24789104›Full record

ArticlePloS one2014

Metformin inhibits the IL-6-induced epithelial-mesenchymal transition and lung adenocarcinoma growth and metastasis.

Zhongquan Zhao, Xiaoming Cheng, Yubo Wang, Rui Han, Li Li, Tong Xiang, Luhang He, Haixia Long, Bo Zhu, Yong He

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  7. Article
  8. Review
  9. Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024
    Review
  10. Review
  11. Article
  12. Association of Elevated Expression Levels ofJournal of personalized medicine · 2022
    Article
  13. Article
  14. Circ_001042 Inhibits TGF-Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
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7 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Zhongquan ZhaoInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China; Department of Oncology, Fuzhhou General Hospital of Nanjing Military Commond, Fuzhou, China.
Xiaoming ChengInstitute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Yubo WangDepartment of Respiratory Medicine, Daping hospital, Third Military Medical University, Chongqing, China.
Rui HanDepartment of Respiratory Medicine, Daping hospital, Third Military Medical University, Chongqing, China.
Li LiDepartment of Respiratory Medicine, Daping hospital, Third Military Medical University, Chongqing, China.
Tong XiangInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Luhang HeInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Haixia LongInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Bo ZhuInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China; Biomedical Analysis Center, Third Military Medical University, Chongqing, China.
Yong HeDepartment of Respiratory Medicine, Daping hospital, Third Military Medical University, Chongqing, China.
Army Medical University · CNXinqiao Hospital · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveEpithelial-mesenchymal transition (EMT) plays an important role in cancer tumorigenesis. However, the underlying mechanisms of EMT in lung adenocarcinoma, and how this process might be inhibited, remain to be explored. This study investigated the role of IL-6 in lung adenocarcinoma cell EMT and explored the potential effects of metformin on this process.

methodsInvasion assay and MTT assay was performed to determine cell invasion and cell proliferation. Western blotting, immunofluorescence, real-time PCR, ELISA, and immunohistochemistry were performed to detect the expression of IL-6, E-cadherin, Vimentin, and p-STAT3.

resultsWe discovered that IL-6, via STAT3 phosphorylation, could promote lung adenocarcinoma cell invasion via EMT in vitro. This was supported by the inverse correlation between E-cadherin and IL-6 expression, positive correlation between IL-6 and vimentin mRNA expression and between STAT3 phosphorylation and IL-6 expression in tumor tissues. Importantly, metformin inhibited tumor growth and distant metastases in tumor-bearing nude mice and reversed IL-6-induced EMT both in vitro and in vivo. Furthermore, we found that blockade of STAT3 phosphorylation might be the underlying mechanism of metformin inhibition of IL-6-induced EMT.

conclusionsCollectively, our present results show that enhanced IL-6 expression, via STAT3 phosphorylation, is a mechanism of EMT in lung adenocarcinoma. We found that metformin could inhibit IL-6-induced EMT possibly by blocking STAT3 phosphorylation.

Indexed as

AdenocarcinomaBlotting, WesternCell DivisionCell Line, TumorEnzyme-Linked Immunosorbent AssayEpithelial-Mesenchymal TransitionHumansInterleukin-6Lung NeoplasmsMetforminNeoplasm MetastasisPhosphorylationReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionSTAT3 Transcription FactorInterleukin-6MetforminSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID24789104
PMCPMC4005743
OpenAlexW2039152216

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.