Evidence map›Paper›PMID 22527937›Full record

ArticleMolecular and cellular biochemistry2012

Apigenin induces apoptosis via extrinsic pathway, inducing p53 and inhibiting STAT3 and NFκB signaling in HER2-overexpressing breast cancer cells.

Hye-Sook Seo, Han-Seok Choi, Soon-Re Kim, Youn Kyung Choi, Sang-Mi Woo, Incheol Shin, Jong-Kyu Woo, Sang-Yoon Park, Yong Cheol Shin, Seong-Gyu Ko and 1 more

Erratum issuedAbstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.2field-weighted citation impact, top 7% 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, 104 citations in OpenAlex.

  1. Review
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  6. Apigenin Ameliorates HPharmaceuticals (Basel, Switzerland) · 2024
    Article
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  10. Phytochemical Constituents and Derivatives ofInternational journal of molecular sciences · 2023
    Review
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4 · The record

Corrections and comments

  • Erratum issued
    Ko, Seong-Kyu [corrected to Ko, Seong-Gyu]
5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Hye-Sook SeoLaboratory of Clinical Biology and Pharmacogenomics and Center for Clinical Research and Genomics, Institute of Oriental Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.
Han-Seok Choi
Soon-Re Kim
Youn Kyung Choi
Sang-Mi Woo
Incheol Shin
Jong-Kyu Woo
Sang-Yoon Park
Yong Cheol Shin
Seong-Gyu Ko
Seong-Kyu Ko
Kyung Hee University · KRHanyang University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phytoestrogens are known to prevent tumor induction. But their molecular mechanisms of action are still unknown. This study aimed to examine the effect of apigenin on proliferation and apoptosis in HER2-expressing breast cancer cells. In our experiments, apigenin inhibited the proliferation of MCF-7 vec and MCF-7 HER2 cells. This growth inhibition was accompanied with an increase of sub G(0)/G(1) apoptotic fractions. Overexpression of HER2 did not confer resistance to apigenin in MCF-7 cells. Apigenin-induced extrinsic apoptosis pathway up-regulating the levels of cleaved caspase-8, and inducing the cleavage of poly (ADP-ribose) polymerase, whereas apigenin did not induce apoptosis via intrinsic mitochondrial apoptosis pathway since this compound did not decrease mitochondrial membrane potential maintaining red fluorescence and did not affect the levels of B-cell lymphoma 2 (BCL2) and Bcl-2-associated X protein. Moreover, apigenin reduced the tyrosine phosphorylation of HER2 (phospho-HER2 level) in MCF-7 HER2 cells, and up-regulated the levels of p53, phospho-p53 and p21 in MCF-7 vec and MCF-7 HER2 cells. This suggests that apigenin induces apoptosis through p53-dependent pathway. Apigenin also reduced the expression of phospho-JAK1 and phospho-STAT3 and decreased STAT3-dependent luciferase reporter gene activity in MCF-7 vec and MCF-7 HER2 cells. Apigenin decreased the phosphorylation level of IκBα in the cytosol, and abrogated the nuclear translocation of p65 within the nucleus suggesting that it blocks the activation of NFκB signaling pathway in MCF-7 vec and MCF-7 HER2 cells. Our study indicates that apigenin could be a potential useful compound to prevent or treat HER2-overexpressing breast cancer.

Indexed as

Antineoplastic Agents, PhytogenicApigeninApoptosisApoptosis Regulatory ProteinsBreast NeoplasmsCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleG1 Phase Cell Cycle CheckpointsGene Expression ProfilingHumansIntracellular Signaling Peptides and ProteinsMembrane Potential, MitochondrialNF-kappa BPhytoestrogensAntineoplastic Agents, PhytogenicApigeninApoptosis Regulatory ProteinsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesIntracellular Signaling Peptides and ProteinsNF-kappa BPhytoestrogensSTAT3 protein, humanSTAT3 Transcription FactorTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22527937
OpenAlexW2007453791

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.