Evidence map›Paper›PMID 31821701›Full record

ArticleJournal of cellular and molecular medicine2020

Lovastatin-mediated MCF-7 cancer cell death involves LKB1-AMPK-p38MAPK-p53-survivin signalling cascade.

Shiu-Wen Huang, I-Tsu Chyuan, Ching Shiue, Meng-Chieh Yu, Ya-Fen Hsu, Ming-Jen Hsu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Review
  5. 27-Hydroxycholesterol in cancer development and drug resistance.Journal of enzyme inhibition and medicinal chemistry · 2025
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  7. Drug repurposing in oncology: a path beyond the bottleneck.Medical oncology (Northwood, London, England) · 2025
    Review
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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

6 authors at 5 institutions in 1 country.

Shiu-Wen HuangDepartment of Medical Research, Taipei Medical University Hospital, Taipei, Taiwan.
I-Tsu ChyuanDepartment of Internal Medicine, Cathay General Hospital, Taipei, Taiwan.
Ching ShiueGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Meng-Chieh YuDepartment of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Ya-Fen HsuDivision of General Surgery, Department of Surgery, Landseed Hospital, Taoyuan, Taiwan.
Ming-Jen HsuDepartment of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.ORCID 0000-0001-9688-8494
Taipei Medical University · TWFu Jen Catholic University · TWLandseed Hospital · TWTaipei Medical University Hospital · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is increasing evidence that statins, which are widely used in lowering serum cholesterol and the incidence of cardiovascular diseases, also exhibits anti-tumour properties. The underlying mechanisms by which statins-induced cancer cell death, however, remain incompletely understood. In this study, we explored the anti-tumour mechanisms of a lipophilic statin, lovastatin, in MCF-7 breast cancer cells. Lovastatin inhibited cell proliferation and induced cell apoptosis. Lovastatin caused p21 elevation while reduced cyclin D1 and survivin levels. Lovastatin also increased p53 phosphorylation, acetylation and its reporter activities. Results from chromatin immunoprecipitation analysis showed that p53 binding to the survivin promoter region was increased, while Sp1 binding to the region was decreased, in MCF-7 cells after lovastatin exposure. These actions were associated with liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (p38MAPK) activation. Lovastatin's enhancing effects on p53 activation, p21 elevation and survivin reduction were significantly reduced in the presence of p38MAPK signalling inhibitor. Furthermore, LKB1-AMPK signalling blockade abrogated lovastatin-induced p38MAPK and p53 phosphorylation. Together these results suggest that lovastatin may activate LKB1-AMPK-p38MAPK-p53-survivin cascade to cause MCF-7 cell death. The present study establishes, at least in part, the signalling cascade by which lovastatin induces breast cancer cell death.

Indexed as

Signal TransductionAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesApoptosisCell DeathCell ProliferationCell SurvivalCyclin-Dependent Kinase Inhibitor p21HumansLovastatinMCF-7 Cellsp38 Mitogen-Activated Protein KinasesPhosphorylationProtein Serine-Threonine KinasesSurvivinTumor Suppressor Protein p53AMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesCyclin-Dependent Kinase Inhibitor p21Lovastatinp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesSTK11 protein, humanSurvivinTumor Suppressor Protein p53breast cancerliver kinase B1lovastatinp53surviving

Identifiers

PMID31821701
PMCPMC6991643
OpenAlexW2996392032

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.