Evidence map›Paper›PMID 25885018›Full record

ArticleBMC cancer2015

The natural compound Guttiferone F sensitizes prostate cancer to starvation induced apoptosis via calcium and JNK elevation.

Xin Li, Yuanzhi Lao, Hong Zhang, Xiaoyu Wang, Hongsheng Tan, Zhixiu Lin, Hongxi Xu

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. 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
8.8field-weighted citation impact, top 3% 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, 40 citations in OpenAlex.

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  13. Dietary restriction: could it be considered as speed bump on tumor progression road?Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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  17. Allanblackia Oil: Phytochemistry and Use as a Functional Food.International journal of molecular sciences · 2015
    Review
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 2 institutions in 1 country.

Xin LiSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, P.R. China. lixin458468@126.com.
Yuanzhi LaoSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, P.R. China. Laurence_ylao@163.com.
Hong ZhangSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, P.R. China. zhnjau19851010@163.com.
Xiaoyu WangSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, P.R. China. wangdxiaoyu@hotmail.com.
Hongsheng TanSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, P.R. China. ths97029@163.com.
Zhixiu LinSchool of Chinese Medicine, Faculty of Science, The Chinese University of Hong Kong, Shatin, N.T, Hong Kong, SAR, China. linzx@cuhk.edu.hk.
Hongxi XuSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, P.R. China. xuhongxi88@gmail.com.
Shanghai University of Traditional Chinese Medicine · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn a cytotoxicity screen in serum-free medium, Guttiferone F showed strong growth inhibitory effect against prostate cancer cells.

methodsProstate cancer cells LNCaP and PC3 were treated with Guttiferone F in serum depleted medium. Sub-G1 phase distributions were estimated with flow cytometry. Mitochondrial disruption was observed under confocal microscope using Mitotracker Red staining. Gene and protein expression changes were detected by real-time PCR and Western blotting. Ca(2+) elevation was examined by Fluo-4 staining under fluorescence microscope. PC3 xenografts in mice were examined by immunohistochemical analysis.

resultsGuttiferone F had strong growth inhibitory effect against prostate cancer cell lines under serum starvation. It induced a significant increase in sub-G1 fraction and DNA fragmentation. In serum-free medium, Guttiferone F triggered mitochondria dependent apoptosis by regulating Bcl-2 family proteins. In addition, Guttiferone F attenuated the androgen receptor expression and phosphorylation of ERK1/2, while activating the phosphorylation of JNK and Ca(2+) flux. Combination of caloric restriction with Guttiferone F in vivo could increase the antitumor effect without causing toxicity.

conclusionsGuttiferone F induced prostate cancer cell apoptosis under serum starvation via Ca(2+) elevation and JNK activation. Combined with caloric restriction, Guttiferone F exerted significant growth inhibition of PC3 cells xenograft in vivo. Guttiferone F is therefore a potential anti-cancer compound.

Indexed as

Caloric RestrictionAnimalsAntineoplastic Agents, PhytogenicApoptosisBenzophenonesBiological ProductsCalciumCaspasesCell Line, TumorCell ProliferationCytosolDisease Models, AnimalHumansJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemAntineoplastic Agents, PhytogenicBenzophenonesBiological ProductsCalciumCaspasesguttiferone FJNK Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2Receptors, Androgen

Identifiers

PMID25885018
PMCPMC4394563
OpenAlexW1992138428

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.