Evidence map›Paper›PMID 33680016›Full record

ArticleIranian journal of pharmaceutical research : IJPR2020

Naringenin Enhances the Anti-Cancer Effect of Cyclophosphamide against MDA-MB-231 Breast Cancer Cells Via Targeting the STAT3 Signaling Pathway.

Shokoofe Noori, Mostafa Rezaei Tavirani, Niloofar Deravi, Mohammad Ismaiil Mahboobi Rabbani, Afshin Zarghi

Abstract read
In one paragraph

Article in Iranian journal of pharmaceutical research : IJPR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

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  8. Naringin vs.Antioxidants (Basel, Switzerland) · 2025
    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

5 authors.

Shokoofe NooriDepartment of Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mostafa Rezaei TaviraniProteomics Research Center, School of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Niloofar DeraviDepartment of Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad Ismaiil Mahboobi RabbaniDepartment of Pharmaceutical Chemistry, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Afshin ZarghiDepartment of Pharmaceutical Chemistry, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Naringenin is a natural compound with potential anti-cancer effects against several cancer types. Also, its precise molecular mechanisms regarding tumor growth suppression has not been completely elucidated. In the current study the apoptosis-inducing and anti-proliferative effects of Naringenin together with cyclophosphamide were studied in breast cancer cells and the participation of JAK2/STAT3 pathway was investigated. In this regard, MDA-MB-231 breast cancer cells were cultured and hence, treated with different concentrations of Naringenin. Apoptosis was measured via flowcytometric analysis of annexin V binding and cell viability was assessed via MTT assay. Protein and gene expression were investigated via Western blotting and real-time PCR, respectively. The function of caspase enzymes were also assessed. The results exhibited that Naringenin triggered apoptosis and markedly decreased cell viability. Furthermore its coadministration with cyclophosphamide improved its anti-tumor properties. Moreover, Naringenin up-regulated the expression of BAX while decreased the expression of Bcl-2. Caspases 3 and 9 were activated by Naringenin, an influence, which was augmented via cyclophosphamide. Docking studies revealed an interaction between Naringenin and STAT3 that was confirmed via attenuation of STAT3 phosphorylation subsequent to treating the cells with Naringenin. Furthermore, Naringenin exhibited the capacity to suppress the function of IL-6 in modulating apoptosis-associated genes expression. Overall, these results indicated that a Naringenin- cyclophosphamide combination impairs proliferation signaling and induces apoptosis to a greater extent than either compound alone and can serve as a potent chemotherapeutic regimen for breast cancer treatment.

Indexed as

ApoptosisBreast cancerCyclophosphamideNaringeninSTAT3

Identifiers

PMID33680016
PMCPMC7757999

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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.