Evidence map›Paper›PMID 35406599›Full record

ArticleCancers2022

Anticancer Effects and Molecular Mechanisms of Apigenin in Cervical Cancer Cells.

Ya-Hui Chen, Jyun-Xue Wu, Shun-Fa Yang, Chueh-Ko Yang, Tze-Ho Chen, Yi-Hsuan Hsiao

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 66 citations in OpenAlex.

  1. Targeting Cancer Hallmarks withInternational journal of molecular sciences · 2026
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  8. Food science & nutrition · 2026
    Review
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  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
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  18. Potential anticancer effects and toxicity of flavones luteolin and apigeninJournal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
    Review
  19. Review
  20. 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

6 authors at 3 institutions in 1 country.

Ya-Hui ChenWomen's Health Research Laboratory, Changhua Christian Hospital, Changhua 50006, Taiwan.
Jyun-Xue WuWomen's Health Research Laboratory, Changhua Christian Hospital, Changhua 50006, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.ORCID 0000-0002-0365-7927
Chueh-Ko YangWomen's Health Research Laboratory, Changhua Christian Hospital, Changhua 50006, Taiwan.
Tze-Ho ChenDepartment of Obstetrics and Gynecology, Changhua Christian Hospital, Changhua 50006, Taiwan.
Yi-Hsuan HsiaoWomen's Health Research Laboratory, Changhua Christian Hospital, Changhua 50006, Taiwan.
Changhua Christian Hospital · TWChung Shan Medical University Hospital · TWKaohsiung Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer is the fourth most frequent malignancy in women. Apigenin is a natural plant-derived flavonoid present in common fruit, vegetables, and herbs, and has been found to possess antioxidant and anti-inflammatory properties as a health-promoting agent. It also exhibits important anticancer effects in various cancers, but its effects are not widely accepted by clinical practitioners. The present study investigated the anticancer effects and molecular mechanisms of apigenin in cervical cancer in vitro and in vivo. HeLa and C33A cells were treated with different concentrations of apigenin. The effects of apigenin on cell viability, cell cycle distribution, migration potential, phosphorylation of PI3K/AKT, the integrin β1-FAK signaling pathway, and epithelial-to-mesenchymal transition (EMT)-related protein levels were investigated. Mechanisms identified from the in vitro study were further validated in a cervical tumor xenograft mouse model. Apigenin effectively inhibited the growth of cervical cancer cells and cervical tumors in xenograft mice. Furthermore, the apigenin down-regulated FAK signaling (FAK, paxillin, and integrin β1) and PI3K/AKT signaling (PI3K, AKT, and mTOR), inactivated or activated various signaling targets, such as Bcl-2, Bax, p21

Indexed as

apigeninapoptosiscervical cancerEMTintegrin β1-FAKPI3K/AKT

Identifiers

PMID35406599
PMCPMC8998024
OpenAlexW4223424947

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.