Evidence map›Paper›PMID 29179721›Full record

ArticleJournal of experimental & clinical cancer research : CR2017

Apigenin, by activating p53 and inhibiting STAT3, modulates the balance between pro-apoptotic and pro-survival pathways to induce PEL cell death.

Marisa Granato, Maria Saveria Gilardini Montani, Roberta Santarelli, Gabriella D'Orazi, Alberto Faggioni, Mara Cirone

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.8field-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

52 citing papers in PubMed, 77 citations in OpenAlex.

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  17. Antitumor Effects of MicroencapsulatedMaterials (Basel, Switzerland) · 2023
    Article
  18. An Update on the Therapeutic Anticancer Potential ofMolecules (Basel, Switzerland) · 2023
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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

6 authors at 2 institutions in 1 country.

Marisa GranatoDepartment of Experimental Medicine, "Sapienza" University of Rome, Viale Regina Elena 324, 00161, Rome, Italy.
Maria Saveria Gilardini MontaniDepartment of Experimental Medicine, "Sapienza" University of Rome, Viale Regina Elena 324, 00161, Rome, Italy.
Roberta SantarelliDepartment of Experimental Medicine, "Sapienza" University of Rome, Viale Regina Elena 324, 00161, Rome, Italy.
Gabriella D'OraziDepartment of Research, Advanced Diagnostics, and Technological Innovation, Regina Elena National Cancer Institute, 00144, Rome, Italy.
Alberto FaggioniDepartment of Experimental Medicine, "Sapienza" University of Rome, Viale Regina Elena 324, 00161, Rome, Italy. alberto.faggioni@uniroma1.it.
Mara CironeDepartment of Experimental Medicine, "Sapienza" University of Rome, Viale Regina Elena 324, 00161, Rome, Italy. mara.cirone@uniroma1.it.
Sapienza University of Rome · ITUniversity of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApigenin is a flavonoid widely distributed in plant kingdom that exerts cytotoxic effects against a variety of solid and haematological cancers. In this study, we investigated the effect of apigenin against primary effusion lymphoma (PEL), a KSHV-associated B cell lymphoma characterized by a very aggressive behavior, displaying constitutive activation of STAT3 as well as of other oncogenic pathways and harboring wtp53.

methodsCell death was assessed by trypan blue exclusion assay, FACS analysis as well as by biochemical studies. The latter were also utilized to detect the occurrence of autophagy and the molecular mechanisms leading to the activation of both processes by apigenin. FACS analysis was used to measure the intracellular ROS utilizing DCFDA.

resultsWe show that apigenin induced PEL cell death and autophagy along with reduction of intracellular ROS. Mechanistically, apigenin activated p53 that induced catalase, a ROS scavenger enzyme, and inhibited STAT3, the most important pro-survival pathway in PEL, as assessed by p53 silencing. On the other hand, STAT3 inhibition by apigenin resulted in p53 activation, since STAT3 negatively influences p53 activity, highlighting a regulatory loop between these two pathways that modulates PEL cell death/survival.

conclusionThe findings of this study demonstrate that apigenin may modulate pro-apoptotic and pro-survival pathways representing a valid therapeutic strategy against PEL.

Indexed as

Antineoplastic Agents, PhytogenicApigeninApoptosisAutophagyCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansLymphoma, Primary EffusionPhosphorylationReactive Oxygen SpeciesSTAT3 Transcription FactorTumor Suppressor Protein p53Antineoplastic Agents, PhytogenicApigeninReactive Oxygen SpeciesSTAT3 protein, humanSTAT3 Transcription FactorTP53 protein, humanTumor Suppressor Protein p53ApigeninApoptosisAutophagyKSHVp53PELSTAT3vFLIP

Identifiers

PMID29179721
PMCPMC5704516
OpenAlexW2770648319

What OpenQuestion holds

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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.