Evidence map›Paper›PMID 25190016›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

Inducing apoptosis effect of caffeic acid 3,4-dihydroxy-phenethyl ester on the breast cancer cells.

Jiaoyuan Jia, Mei Yang, Yu Chen, Hongyan Yuan, Jinghe Li, Xueling Cui, Zhonghui Liu

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Platinum-zoledronate complex blocks gastric cancer cell proliferation by inducing cell cycle arrest and apoptosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  3. Article
  4. Article
  5. 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

7 authors at 4 institutions in 1 country.

Jiaoyuan JiaDepartment of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, 130041, China.
Mei Yang
Yu Chen
Hongyan Yuan
Jinghe Li
Xueling Cui
Zhonghui Liu
Jilin Medical University · CNJilin University · CNSecond Affiliated Hospital of Jilin University · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To explore the antitumor effect of caffeic acid 3,4-dihydroxy-phenethyl ester (CADPE) on the breast cancer cell lines and illuminate the related mechanism. After treatment with different concentrations of CADPE for 24, 48, and 72 h, cell proliferation ability of the breast cancer cell lines MDA-MB-231 and MDA-MB-435 was analyzed by the MTT. Changes of the cell cycles were evaluated by PI staining. Cell apoptosis was examined by flow cytometry after Annexin V/7AAD double staining. Nuclear morphologic changes were observed under the inverted fluorescence microscope after staining with Hoechst 33342. Mitochondrial membrane potential and reactive oxygen species (ROS) level were estimated by JC-1 and DCFH-DA staining. In addition, the expression level of mitochondrial signaling pathway proteins Bcl-2, Bax, and caspase-3 were evaluated by Western blot. CADPE has the distinct cytotoxic effect to the breast cancer cells, and the effect is dose dependent. It did not change the cell cycles but induced the cell apoptosis of the breast cancer cells. At the same time, after CADPE treatment, the expression levels of caspase-3 and Bax in the breast cancer cells were upregulated and Bcl-2 expression was declined. The ROS level in the breast cancer cells was enhanced, and mitochondrial membrane potential of the cells was downregulated. CADPE has the antitumor functions. It can induce the cell apoptosis through downregulating Bcl-2 expression, enhancing Bax and caspase-3 expression levels, upregulating ROS level and reducing the mitochondrial membrane potential of the breast cancer cells to trigger the mitochondrial signal pathway.

Indexed as

Apoptosisbcl-2-Associated X ProteinBreast NeoplasmsCaffeic AcidsCaspase 3Cell CycleCell Line, TumorCell ProliferationCells, CulturedFemaleHumansMembrane Potential, MitochondrialMitochondriaProto-Oncogene Proteins c-bcl-2Reactive Oxygen Species3-(3,4-dihydroxyphenyl)acrylic acid 2-(3,4-dihydroxyphenyl)ethyl esterbcl-2-Associated X ProteinCaffeic AcidsCaspase 3Proto-Oncogene Proteins c-bcl-2Reactive Oxygen Species

Identifiers

PMID25190016
OpenAlexW2071776543

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.