Evidence map›Paper›PMID 33052427›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2021

Dual targeting of Notch and Wnt/β-catenin pathways: Potential approach in triple-negative breast cancer treatment.

Fatma Nasser, Nermine Moussa, Maged W Helmy, Medhat Haroun

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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

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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.

Fatma NasserDepartment of Biotechnology, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt.
Nermine MoussaDepartment of Biotechnology, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt. igsr.nerminemoussa@alexu.edu.eg.
Maged W HelmyFaculty of Pharmacy, Department of Pharmacology and Toxicology, Damanhur University, Damanhur, Egypt.
Medhat HarounDepartment of Biotechnology, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt.
Alexandria University · EGDamanhour University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the continuously growing repertoire of new and improved anti-cancer therapies, triple-negative breast cancer (TNBC) remains a clinical challenge to treat. In this sense, targeting signaling pathways such as Notch and Wnt/β-catenin have attracted growing attention. This work aimed at investigating the possible antitumor effects of IMR-1 as a Notch inhibitor, PRI-724 as a Wnt/β-catenin inhibitor, as well as their combination and to explore the possible crosstalk between Notch and Wnt/β-catenin signaling pathways in MDA-MB-231 TNBC cell line. Microculture tetrazolium test (MTT) was used to determine the drug growth inhibition (GI50), and the results were analyzed using CompuSyn 3.0.1 software. MDA-MB-231 cells were divided into four treatment groups including positive control, IMR-1-treated, PRI-724-treated, and combination-treated groups. Sandwich enzyme-linked immunosorbent assay (ELISA) was used for the determination of the protein levels of hairy and enhancer of split-1 (HES-1), Notch-1, β-catenin, cyclin-D1, and vascular endothelial growth factor (VEGF1). HES-1 gene expression was assessed by quantitative real-time polymerase chain reaction. Statistical analyses were performed using GraphPad Prism Software. The GI50 for IMR-1 and PRI-724 were 15.3 μM and 0.69 μM, respectively. Upon treatment of MDA-MB-231 cells with these drugs, HES-1 gene expression was up-regulated due to single and combined treatments. Moreover, the protein levels of cyclin-D1, VEGF1, HES-1, and Notch-1 were reduced, while those of active β-catenin and active caspase-3 were elevated. IMR-1/PRI-724 combination augmented IMR-1- and PRI-724-mediated effects on MDA-MB-231 cells by initiating apoptotic cell death. Further in vitro and in vivo studies are warranted to support our findings.

Indexed as

Antineoplastic AgentsApoptosisbeta CateninBridged Bicyclo Compounds, HeterocyclicCaspase 3Cell Line, TumorCell ProliferationCyclin D1Drug InteractionsHumansPyrimidinonesReceptor, Notch1ThiazolidinesTranscription Factor HES-1Triple Negative Breast NeoplasmsVascular Endothelial Growth Factor AAntineoplastic Agentsbeta CateninBridged Bicyclo Compounds, HeterocyclicCASP3 protein, humanCaspase 3CCND1 protein, humanCyclin D1HES1 protein, humanICG 001IMR-1 compoundNOTCH1 protein, humanPyrimidinonesReceptor, Notch1ThiazolidinesTranscription Factor HES-1Vascular Endothelial Growth Factor AVEGFA protein, humanIMR-1Notch pathwayPRI-724Triple-negative breast cancerWnt/β-catenin pathway

Identifiers

PMID33052427
OpenAlexW3092285135

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.