Evidence map›Paper›PMID 24335836›Full record

ArticleActa pharmacologica Sinica2014

Bornyl caffeate induces apoptosis in human breast cancer MCF-7 cells via the ROS- and JNK-mediated pathways.

Chuan-bin Yang, Wei-jing Pei, Jia Zhao, Yuan-yuan Cheng, Xiao-hui Zheng, Jian-hui Rong

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

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  7. Review
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  9. JNK signaling as a target for anticancer therapy.Pharmacological reports : PR · 2021
    Review
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  14. Review
  15. Releasing Nrf2 to promote neurite outgrowth.Neural regeneration research · 2015
    Article
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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 3 institutions in 2 countries.

Chuan-bin YangSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Wei-jing PeiRITS and NWU Joint Laboratory for New Drugs Research of TCM, Research Institute of Tsinghua University in Shenzhen, Shenzhen 518000, China.
Jia ZhaoSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Yuan-yuan ChengSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Xiao-hui Zheng1] RITS and NWU Joint Laboratory for New Drugs Research of TCM, Research Institute of Tsinghua University in Shenzhen, Shenzhen 518000, China [2] Key Laboratory of Resource Biology and Biotechnology in Western China, School of Life Sciences, Northwest University, Xi'an 710069, China.
Jian-hui RongSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Chinese University of Hong Kong · CNTsinghua University · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThe purpose of the present study was to investigate the anticancer activity of bornyl caffeate in the human breast cancer cell line MCF-7.

methodsThe cell viability was determined using the MTT assay, and apoptosis was initially defined by monitoring the morphology of the cell nuclei and staining an early apoptotic biomarker with Annexin V-FITC. The mitochondrial membrane potential was visualized by JC-1 under fluorescence microscopy, whereas intracellular reactive oxygen species (ROS) were assessed by flow cytometry. The expression of apoptosis-associated proteins was determined by Western blotting analysis.

resultsBornyl caffeate induced apoptosis in MCF-7 cells in a dose- and time-dependent manner. Consistently, bornyl caffeate increased Bax and decreased Bcl-xl, resulting in the disruption of MMP and subsequent activation of caspase-3. Moreover, bornyl caffeate triggered the formation of ROS and the activation of the mitogen-activated protein (MAP) kinases p38 and c-Jun N-terminal kinase (JNK). Antioxidants attenuated the activation of MAP kinase p38 but barely affected the activation of JNK. Importantly, the cytotoxicity of bornyl caffeate was partially attenuated by scavenging ROS and inhibited by MAP kinases and caspases.

conclusionThe present study demonstrated that bornyl caffeate induced apoptosis in the cancer cell line MCF-7 via activating the ROS- and JNK-mediated pathways. Thus, bornyl caffeate may be a potential anticancer lead compound.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBreast NeoplasmsCoumaric AcidsDose-Response Relationship, DrugFemaleHeLa CellsHep G2 CellsHumansMAP Kinase Signaling SystemMCF-7 CellsPC12 CellsRatsReactive Oxygen SpeciesAntineoplastic Agentsbornyl caffeateCoumaric AcidsReactive Oxygen Species

Identifiers

PMID24335836
PMCPMC4075736
OpenAlexW1990216025

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.