Evidence map›Paper›PMID 24960186›Full record

ArticlePloS one2014

Caffeic acid derivatives inhibit the growth of colon cancer: involvement of the PI3-K/Akt and AMPK signaling pathways.

En-Pei Isabel Chiang, Shu-Yao Tsai, Yueh-Hsiung Kuo, Man-Hui Pai, Hsi-Lin Chiu, Raymond L Rodriguez, Feng-Yao Tang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.9field-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

51 citing papers in PubMed, 110 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

7 authors at 5 institutions in 2 countries.

En-Pei Isabel ChiangDepartment of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan, Republic of China; NCHU-UCD Plant and Food Biotechnology Program and Agricultural Biotechnology Center, National Chung Hsing University, Taichung, Taiwan, Republic of China.
Shu-Yao TsaiDepartment of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan, Republic of China.
Yueh-Hsiung KuoDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan, Republic of China; Department of Biotechnology, Asia University, Taichung, Taiwan, Republic of China.
Man-Hui PaiDepartment of Anatomy, Taipei Medical University, Taipei, Taiwan, Republic of China.
Hsi-Lin ChiuDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan, Republic of China; Department of Biotechnology, Asia University, Taichung, Taiwan, Republic of China.
Raymond L RodriguezDepartment of Molecular and Cellular Biology, University of California Davis, Davis, California, United States of America.
Feng-Yao TangBiomedical Science Laboratory, Department of Nutrition, China Medical University, Taichung, Taiwan, Republic of China.
China Medical University · TWAsia University · TWNational Chung Hsing University · TWTaipei Medical University · TWUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aberrant regulation of phosphatidylinositide 3-kinases (PI3-K)/Akt, AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (m-TOR) signaling pathways in cancer has prompted significant interest in the suppression of these pathways to treat cancer. Caffeic acid (CA) has been reported to possess important anti-inflammatory actions. However, the molecular mechanisms by which CA derivatives including caffeic acid phenethyl ester (CAPE) and caffeic acid phenylpropyl ester (CAPPE), exert inhibitory effects on the proliferation of human colorectal cancer (CRC) cells have yet to be elucidated. METHODOLOGY/PRINCIPAL

findingsCAPE and CAPPE were evaluated for their ability to modulate these signaling pathways and suppress the proliferation of CRC cells both in vitro and in vivo. Anti-cancer effects of these CA derivatives were measured by using proliferation assays, cell cycle analysis, western blotting assay, reporter gene assay and immunohistochemical (IHC) staining assays both in vitro and in vivo. This study demonstrates that CAPE and CAPPE exhibit a dose-dependent inhibition of proliferation and survival of CRC cells through the induction of G0/G1 cell cycle arrest and augmentation of apoptotic pathways. Consumption of CAPE and CAPPE significantly inhibited the growth of colorectal tumors in a mouse xenograft model. The mechanisms of action included a modulation of PI3-K/Akt, AMPK and m-TOR signaling cascades both in vitro and in vivo. In conclusion, the results demonstrate novel anti-cancer mechanisms of CA derivatives against the growth of human CRC cells.

conclusionsCA derivatives are potent anti-cancer agents that augment AMPK activation and promote apoptosis in human CRC cells. The structure of CA derivatives can be used for the rational design of novel inhibitors that target human CRC cells.

Indexed as

Antineoplastic AgentsCaffeic AcidsCell Cycle CheckpointsCell Line, TumorCell ProliferationColonic NeoplasmsHCT116 CellsHumansMAP Kinase Signaling SystemPhenylethyl Alcohol3-phenylpropyl caffeateAntineoplastic Agentscaffeic acid phenethyl esterCaffeic AcidsPhenylethyl Alcohol

Identifiers

PMID24960186
PMCPMC4069067
OpenAlexW2062172769

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.