Evidence map›Paper›PMID 25859163›Full record

ArticleCancer cell international2015

Apigenin, a dietary flavonoid, inhibits proliferation of human bladder cancer T-24 cells via blocking cell cycle progression and inducing apoptosis.

Ming-Der Shi, Cheng-Kai Shiao, Yi-Chieh Lee, Yuan-Wei Shih

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
6.0field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 114 citations in OpenAlex.

  1. The Role of Natural Compounds in Bladder Urothelial Carcinoma Treatment.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Apigenin Suppresses Bladder Cancer via the SIRT6-NCOA2-PPARα Axis.International journal of biological sciences · 2026
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  16. Molecules (Basel, Switzerland) · 2022
    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

4 authors at 2 institutions in 1 country.

Ming-Der ShiDepartment of Medical Technology, Kaohsiung Veterans General Hospital Tainan Branch, Tainan, 71051 Taiwan ; Department of Medical Laboratory Science and Biotechnology and Graduate Institute of Biological Technology, Chung Hwa University of Medical Technology, Tainan, 71703 Taiwan.
Cheng-Kai ShiaoDepartment of Chest Medicine, Kaohsiung Veterans General Hospital Tainan Branch, Tainan, 71051 Taiwan.
Yi-Chieh LeeDepartment of Nursing, Chung Hwa University of Medical Technology, Tainan, 71703 Taiwan.
Yuan-Wei ShihDepartment of Food Nutrition, Chung Hwa University of Medical Technology, Tainan, 71703 Taiwan ; Department of Biological Science and Technology and Graduate Institute of Biomedical Science, Chung Hwa University of Medical Technology, Tainan, 71703 Taiwan.
Chung Hwa University of Medical Technology · TWKaohsiung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApigenin is a nontoxic dietary flavonoid, and it may have chemopreventive and therapeutic potential as an anti-inflammatory, antioxidant, and anti-cancer agent. However, its role in bladder cancer remains poorly understood. The aim of this study was to investigate the anti-proliferative activity of apigenin in human bladder cancer T-24 cells. METHODS AND

resultsApigenin inhibited T-24 cell proliferation in a dose-dependent manner. We demonstrated that apigenin-induced early and mid-apoptotic cell could be identified by Annexnin V-Alexa Fluor 488/PI apoptosis detection and TUNEL assay. Moreover, using a JC-1 staining assay, we found that apigenin may induce the loss of the mitochondrial membrane potential. By performing flow cytometry and Western blotting, apigenin-mediated subG1 phase acculmulation was also associated with an increase in the phospho-p53, p53, p21, and p27 levels, and with a decrease in the Cyclin A, Cyclin B1, Cyclin E, CDK2, Cdc2, and Cdc25C levels, thereby blocking cell cycle progression. ELISA showed that the subG1 phase acculmulation was due to the increase in the p53, p21, and p27 levels. In addition, apigenin increased the Bax, Bad, and Bak levels, but reduced the Bcl-xL, Bcl-2, and Mcl-1 levels, and subsequently triggered the mitochondrial apoptotic pathway (release of cytochrome c and activation of caspase-9, caspase-3, caspase-7, and PARP). Further analysis demonstrated that apigenin increased the ROS levels and depleted GSH in T-24 cells at 12 h.

conclusionsThe results suggested that apigenin inhibits T-24 cells proliferation via blocking cell cycle progression and inducing apoptosis. In addition, we discovered a potential anticancer activity of apigenin against T-24 cells.

Indexed as

ApigeninCaspaseCDKCyclinMitochondrial membrane potential

Identifiers

PMID25859163
PMCPMC4391114
OpenAlexW2165157873

What OpenQuestion holds

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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.