Evidence map›Paper›PMID 30754643›Full record

ArticleInternational journal of molecular sciences2019

Fluoxetine Induces Apoptosis through Extrinsic/Intrinsic Pathways and Inhibits ERK/NF-κB-Modulated Anti-Apoptotic and Invasive Potential in Hepatocellular Carcinoma Cells In Vitro.

Wei-Ting Chen, Fei-Ting Hsu, Yu-Chang Liu, Cheng-Hsien Chen, Li-Cho Hsu, Song-Shei Lin

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
5.1field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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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.

Wei-Ting ChenDepartment of Medical Imaging and Radiological Sciences, Central Taiwan University of Science and Technology, Taichung 406, Taiwan. wt820368@yahoo.com.tw.
Fei-Ting HsuDepartment of Biological Science and Technology, China Medical University, Taichung 404, Taiwan. sakiro920@mail.cmu.edu.tw.
Yu-Chang LiuDepartment of Medical Imaging and Radiological Sciences, Central Taiwan University of Science and Technology, Taichung 406, Taiwan. kevinyc.liu@gmail.com.ORCID 0000-0002-8681-4472
Cheng-Hsien ChenDepartment of Surgery, Show Chwan Memorial Hospital, Changhua 500, Taiwan. picorna@gmail.com.
Li-Cho HsuDivision of Endocrinology and Metabolism, Department of Medicine, National Yang-Ming University Hospital, Yilan 260, Taiwan. hsulc@ymuh.ym.edu.tw.
Song-Shei LinDepartment of Medical Imaging and Radiological Sciences, Central Taiwan University of Science and Technology, Taichung 406, Taiwan. sslin@ctust.edu.tw.
Chang Bing Show Chwan Memorial Hospital · TWCentral Taiwan University of Science and Technology · TWChina Medical University · TWMin-Hwei College of Health Care Management · TWNational Yang Ming Chiao Tung University · TW

Funding

Central Taiwan University of Science and Technology CTU107-P-105Changhua Show Chwan Memorial Hospital RD107069Zuoying Branch of Kaohsiung Armed Forces General Hospital ZBH107-21
6 · The paper itself

Abstract

The aim of the present study was to verify the effects of fluoxetine on dysregulation of apoptosis and invasive potential in human hepatocellular carcinoma (HCC) SK-Hep1 and Hep3B cells. Cells were treated with different concentrations of fluoxetine for different times. MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assays were used for testing the effects of fluoxetine on cell viability. The regulation of apoptosis signaling, and anti-apoptotic, proliferation, and metastasis-associated proteins after fluoxetine treatment were assayed by flow cytometry and Western blotting assay. The detection of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation after fluoxetine treatment was performed by NF-κB reporter gene assay. The results demonstrated that fluoxetine significantly reduced cell viability, cell migration/invasion, NF-κB, extracellular signal-regulated kinases (ERK) activation, and expression of anti-apoptotic (Cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein (C-FLIP), Myeloid cell leukemia-1 (MCL-1), X-Linked inhibitor of apoptosis protein (XAIP), and Survivin), proliferation (Cyclin-D1), angiogenesis (vascular endothelial growth factor (VEGF)), and metastasis-associated proteins (matrix metalloproteinase-9 (MMP-9)). Fluoxetine also significantly induced apoptosis, unregulated extrinsic (activation of first apoptosis signal protein and ligand (Fas/FasL), and caspase-8) and intrinsic (loss of mitochondrial membrane potential (ΔΨm) pathways and increased Bcl-2 homologous antagonist killer (BAK) apoptosis signaling. Taken together, these results demonstrated that fluoxetine induced apoptosis through extrinsic/intrinsic pathways and diminished ERK/NF-κB-modulated anti-apoptotic and invasive potential in HCC cells in vitro.

Indexed as

Antineoplastic AgentsApoptosisCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationCell SurvivalExtracellular Signal-Regulated MAP KinasesFluoxetineGene Expression Regulation, NeoplasticHumansLiver NeoplasmsModels, BiologicalNF-kappa BSignal TransductionAntineoplastic AgentsExtracellular Signal-Regulated MAP KinasesFluoxetineNF-kappa Bapoptosisfluoxetinehuman hepatocellular carcinomaNF-κB

Identifiers

PMID30754643
PMCPMC6386946
OpenAlexW2913081176

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.