Evidence map›Paper›PMID 25854169›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

Metformin inhibits thyroid cancer cell growth, migration, and EMT through the mTOR pathway.

Baiyu Han, Hanzhi Cui, Lei Kang, Xuelin Zhang, Zhitao Jin, Lanmin Lu, Zhongyi Fan

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 3 pooled it
5.0field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 3 syntheses or guidelines pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Associations between Diabetes Mellitus and Selected Cancers.International journal of molecular sciences · 2024
    Review
  11. Metabolic Reprogramming in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2024
    Review
  12. Article
  13. Observational
  14. Diabetes Mellitus and Thyroid Cancers: Risky Correlation, Underlying Mechanisms and Clinical Prevention.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  15. Review
  16. Article
  17. Metformin and long non-coding RNAs in breast cancer.Journal of translational medicine · 2023
    Review
  18. Review
  19. Article
  20. Review

4 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

7 authors at 4 institutions in 1 country.

Baiyu HanDepartment of Endocrinology and Metabolism, The 264 Hospital of PLA, 30 Qiao-Dong Street, Taiyuan, 030000, Shanxi, China.
Hanzhi Cui
Lei Kang
Xuelin Zhang
Zhitao Jin
Lanmin Lu
Zhongyi Fan
Chinese PLA General Hospital · CNPeking University First Hospital · CNSecond Artillery General Hospital of Chinese People's Liberation Army · CNThe 309th Hospital of Chinese People's Liberation Army · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian target of rapamycin (mTOR) signaling pathways have been shown to be activated in thyroid cancer. Recent evidences have demonstrated that the antidiabetic agent metformin, an activator of 5'-AMP-activated protein kinase, can impair the proliferation and migration of cancer cells via inhibition of mTOR. However, the underlying mechanisms remain unclear. In this study, we show that metformin can inhibit mTOR pathway to impair growth and migration of the thyroid cancer cell lines. Cyclin D1 and c-Myc are important regulators of cancer cell growth, and we observed that treatment of thyroid cancer cells with metformin reduced c-Myc and cyclin D1 expression through suppression of mTOR and subsequent inhibition of P70S6K1 and 4E-BP1 phosphorylation. Metformin reduced epithelial to mesenchymal transition (EMT) in thyroid carcinoma cells. Moreover, metformin regulated expression of the EMT-related markers E-cadherin, N-cadherin, and Snail. Additionally, knockdown of TSC2, the upstream regulatory molecule of mTOR pathway, or treatment of rapamycin, the mTOR inhibitor, could abolish the effects of metformin to regulate thyroid cancer cell proliferation, migration, EMT, and mTOR pathway molecules. These results indicate that metformin can suppress the proliferation, migration, and EMT of thyroid cancer cell lines by inhibiting mTOR signaling. These findings suggest that metformin and its molecular targets may be useful in thyroid carcinoma therapy.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMetforminMiceNeoplasm ProteinsSignal TransductionThyroid NeoplasmsTOR Serine-Threonine KinasesXenograft Model Antitumor AssaysMetforminMTOR protein, humanNeoplasm ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID25854169
OpenAlexW2073183536

What OpenQuestion holds

Textmetadata
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.