Evidence map›Paper›PMID 29450133›Full record

ArticleBiochimie open2016

Inhibition of the MAPK pathway alone is insufficient to account for all of the cytotoxic effects of naringenin in MCF-7 breast cancer cells.

Lauren Eanes, Yashomati M Patel

Open access · hybridAbstract read
In one paragraph

Article in Biochimie open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  14. Identification of potential therapeutic target of naringenin in breast cancer stem cells inhibition by bioinformatics andSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021
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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

2 authors at 1 institution in 1 country.

Lauren EanesDepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USA.
Yashomati M PatelDepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USA.
University of North Carolina at Greensboro · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogen receptor (ER) antagonists such as tamoxifen (Tam) have been used successfully to treat ER+ breast cancers for more than 30 years. Unfortunately, long term use of Tam can result in resistance. Tam resistance is associated with the activation of growth factor signaling pathways that promote cell proliferation and survival. The mitogen-activated protein kinase (MAPK), is up-regulated in Tam resistant (Tam-R) cells. Previous studies have reported that the flavanone, naringenin (Nar) can inhibit cell proliferation and induce apoptosis in ER+ breast cancer cells. Furthermore, Nar has been shown to inhibit the MAPK signaling pathways in MCF-7 cells. In this report we investigated whether inhibition of MAPK alone is mediating the effects of Nar on cell proliferation and viability. These studies will determine the mechanism of action of Nar. Tam-R MCF-7 breast cancer cells were treated with Nar or U0126, a MAPK kinase inhibitor. Our studies show that while both U0126 and Nar impaired cell proliferation and viability the combination of U0126 and Nar resulted in greater inhibition of cell viability than either compound alone. It has been previously reported that Nar can bind the ER. Our lab has also shown that Nar localizes ERα to a peri-nuclear region of the cell. Confocal microscopy revealed that in U0126 treated cells ERα displayed an even distribution across the cytoplasm as seen in untreated Tam-R cells. These studies suggest that MAPK is not the only target of Nar.

Indexed as

MAPK signalingNaringeninTamoxifen resistance

Identifiers

PMID29450133
PMCPMC5801822
OpenAlexW2554298471

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.