Evidence map›Paper›PMID 20809206›Full record

ArticleInvestigational new drugs2012

Expression of Nur77 induced by an n-butylidenephthalide derivative promotes apoptosis and inhibits cell growth in oral squamous cell carcinoma.

Po Yen Liu, Jim Jinn-Chyuan Sheu, Po Cheng Lin, Cheng Tung Lin, Ya Jung Liu, Li Ing Ho, Li Fu Chang, Wan Chen Wu, Syue Rong Chen, Jay Chen and 5 more

Abstract read
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In one paragraph

Article in Investigational new drugs, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.4field-weighted citation impact, top 47% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  17. Brain tumor senescence might be mediated by downregulation of S-phase kinase-associated protein 2 via butylidenephthalide leading to decreased cell viability.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
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

15 authors at 7 institutions in 1 country.

Po Yen LiuSchool of Chinese Medicine, China Medical University, Taichung 40402, Taiwan.
Jim Jinn-Chyuan Sheu
Po Cheng Lin
Cheng Tung Lin
Ya Jung Liu
Li Ing Ho
Li Fu Chang
Wan Chen Wu
Syue Rong Chen
Jay Chen
Yeu Chern Harn
Shinn Zong Lin
Chang Hai Tsai
Tzyy Wen Chiou
Horng Jyh Harn
China Medical University · TWChina Medical University Hospital · TWNational Dong Hwa University · TWHualien Armed Forces General Hospital · TWNational Taiwan University · TWTaipei Veterans General Hospital · TWTunghai University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In spite of numerous advances, the 5-year survival rate for head and neck squamous cell cancer has remained largely stagnant and few new anti-tumor drugs have been developed. PCH4, a derivative of n-butylidenephthalide, has been investigated for its anti-tumor effects on oral squamous cell carcinoma (OSCC). The aim of this study was to investigate the anti-tumor mechanism of a potential target gene, Nur77, in OSCC cells, which can be induced by PCH4 treatment. Data show that PCH4 promoted Nur77 translocation from the nucleus to the cytoplasm and induced cell apoptosis in OSCC cells. When Nur77 translocation was blocked, the degree of tumor apoptosis caused by PCH4 was significantly inhibited (p < 0.05). Within the MAPK pathway, PCH4 only induced JNK phosphorylation. Furthermore, treatment with a JNK inhibitor significantly reduced PCH4-induced apoptosis (p < 0.05) and decreased PCH4-induced Nur77 expression (p < 0.05). In a xenograft animal model, administration of PCH4 also showed anti-tumor effects. We have demonstrated that OSCC cells are sensitive to PCH4 and that Nur77 protein translocation from the nucleus to the cytoplasm might be associated with the induction of apoptosis by PCH4. These results indicate that PCH4 may serve as a potential anti-tumor drug for OSCC therapy.

Indexed as

Active Transport, Cell NucleusAnimalsAntineoplastic AgentsApoptosisBenzofuransCarcinoma, Squamous CellCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, DrugEthylaminesFemaleHumansJNK Mitogen-Activated Protein KinasesMiceMice, Inbred BALB CAntineoplastic AgentsBenzofuransbutylidenephthalideEthylaminesJNK Mitogen-Activated Protein KinasesN-(2-(dimethylamino)ethyl)-2-(3-((3-oxoisobenzofuran-1(3H)-ylidene)methyl)phenoxy)acetamideNR4A1 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1Phthalic AnhydridesProtein Kinase InhibitorsRNA, Messenger

Identifiers

PMID20809206
OpenAlexW2000069559

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.