Evidence map›Paper›PMID 27122225›Full record

ArticleScientific reports2016

Lovastatin causes FaDu hypopharyngeal carcinoma cell death via AMPK-p63-survivin signaling cascade.

Chia-Sheng Yen, Jung-Chien Chen, Yi-Fang Chang, Ya-Fen Hsu, Pei-Ting Chiu, Ching Shiue, Yu-Fan Chuang, George Ou, Ming-Jen Hsu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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  12. Statins: a repurposed drug to fight cancer.Journal of experimental & clinical cancer research : CR · 2021
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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

9 authors at 6 institutions in 2 countries.

Chia-Sheng YenDepartment of General Surgery, Chi-Mei Medical Center, Tainan, Taiwan.
Jung-Chien ChenDivision of General Surgery, Department of Surgery, Min-Sheng General Hospital, Taoyuan, Taiwan.
Yi-Fang ChangDivision of Hematology and Oncology, Department of Internal Medicine, MacKay Memorial Hospital, Taipei, Taiwan.
Ya-Fen HsuDivision of General Surgery, Department of Surgery, Landseed Hospital, Taoyuan, Taiwan.
Pei-Ting ChiuGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Ching ShiueDivision of General Surgery, Department of Surgery, Landseed Hospital, Taoyuan, Taiwan.
Yu-Fan ChuangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
George OuDepartment of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Ming-Jen HsuGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Taipei Medical University · TWLandseed Hospital · TWChi Mei Medical Center · TWMackay Memorial Hospital · TWMin Sheng General Hospital · TWUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Statins are used widely to lower serum cholesterol and the incidence of cardiovascular diseases. Growing evidence shows that statins also exhibit beneficial effects against cancers. In this study, we investigated the molecular mechanisms involved in lovastatin-induced cell death in Fadu hypopharyngeal carcinoma cells. Lovastatin caused cell cycle arrest and apoptosis in FaDu cells. Lovastatin increased p21(cip/Waf1) level while the survivin level was decreased in the presence of lovastatin. Survivin siRNA reduced cell viability and induced cell apoptosis in FaDu cells. Lovastatin induced phosphorylation of AMP-activated protein kinase (AMPK), p38 mitogen-activated protein kinase (MAPK) and transcription factor p63. Lovastatin also caused p63 acetylation and increased p63 binding to survivin promoter region in FaDu cells. AMPK-p38MAPK signaling blockade abrogated lovastatin-induced p63 phosphorylation. Lovastatin's enhancing effect on p63 acetylation was reduced in HDAC3- or HDAC4- transfected cells. Moreover, transfection of cells with AMPK dominant negative mutant (AMPK-DN), HDAC3, HDAC4 or p63 siRNA significantly reduced lovastatin's effects on p21(cip/Waf1) and survivin. Furthermore, lovastatin inhibited subcutaneous FaDu xenografts growth in vivo. Taken together, lovastatin may activate AMPK-p38MAPK-p63-survivin cascade to cause FaDu cell death. This study establishes, at least in part, the signaling cascade by which lovastatin induces hypopharyngeal carcinoma cell death.

Indexed as

Cell DeathAMP-Activated Protein KinasesAntineoplastic AgentsCell Line, TumorEpithelial CellsHumansInhibitor of Apoptosis ProteinsLovastatinSignal TransductionSurvivinTranscription FactorsTumor Suppressor ProteinsAMP-Activated Protein KinasesAntineoplastic AgentsBIRC5 protein, humanInhibitor of Apoptosis ProteinsLovastatinSurvivinTP63 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID27122225
PMCPMC4848532
OpenAlexW2344572401

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.