Evidence map›Paper›PMID 29396474›Full record

ArticleCell death & disease2018

Nicotine associated breast cancer in smokers is mediated through high level of EZH2 expression which can be reversed by methyltransferase inhibitor DZNepA.

Kanchan Kumari, Biswajit Das, Amit Adhya, Sanjib Chaudhary, Shantibhusan Senapati, Sandip K Mishra

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

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  6. Cell signaling and epigenetic regulation of nicotine-induced carcinogenesis.Environmental pollution (Barking, Essex : 1987) · 2024
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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 5 institutions in 2 countries.

Kanchan KumariCancer Biology Laboratory, Department of Gene Function and Regulation, Institute of Life Sciences, Bhubaneswar, Odisha, India.
Biswajit DasTumor Microenvironment and Animal Models Laboratory, Department of Translational Research, Institute of Life Sciences, Bhubaneswar, Odisha, India.
Amit AdhyaPathology Department, Hemalata Hospital, Chandrashekharpur Bhubaneswar, Odisha, India.
Sanjib ChaudharyUniversity of Nebraska Medical Center, Nebraska, NE, USA.
Shantibhusan SenapatiTumor Microenvironment and Animal Models Laboratory, Department of Translational Research, Institute of Life Sciences, Bhubaneswar, Odisha, India.
Sandip K MishraCancer Biology Laboratory, Department of Gene Function and Regulation, Institute of Life Sciences, Bhubaneswar, Odisha, India. sandipkmishra@hotmail.com.
Institute of Life Sciences · INHemalata Hospitals and Research Centre · INManipal Academy of Higher Education · INUniversity of Nebraska Medical Center · USUtkal University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies show substantial growth-promoting properties of nicotine (NIC) in cancer, which is a combined outcome of genetic and epigenetic alterations. However, the role of epigenetic modifiers in response to NIC in breast cancer is less studied. In the present study, for the first time we have shown NIC-induced enhanced EZH2 expression. Six pairs of smoking-associated breast cancer patient tissues were analyzed. Samples from smoking breast cancer patients showed distinguished enhanced EZH2 expression in comparison to non-smoking ones. The upregulation in EZH2, which is due to NIC, was further confirmed in breast carcinoma cell lines using 10 µM NIC, 1 µM DZNepA, and EZH2si. The upregulation of EZH2 was concomitant with upregulation in Myc and α9-nAChR. The xenograft of breast cancer cells in BALB/c nude mice in the presence or absence of NIC showed significantly higher tumor uptake in the NIC injected group, which clearly demonstrates the effect of NIC in breast cancer progression. Interestingly, DZNepA considerably suppressed the NIC-mediated tumor growth. CHIP-qPCR assay confirmed the increased Myc enrichment on EZH2 promoter upon NIC treatment, thereby strengthening our findings that there exists an association between NIC, Myc, and EZH2. Overall, the present study identifies a strong association between NIC and EZH2 particularly in the progression of breast cancer in smokers through a novel axis involving nAChR and Myc. Moreover, the findings provide preliminary evidence suggesting potential of high level of EZH2 expression as a prognostic marker in smoking-associated breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticSmokersAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationDisease ProgressionEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsFemaleHumansKi-67 AntigenMethyltransferasesMice, Inbred BALB CMice, NudeNicotineEnhancer of Zeste Homolog 2 ProteinEnzyme InhibitorsEZH2 protein, humanKi-67 AntigenMethyltransferasesNicotineProto-Oncogene Proteins c-myc

Identifiers

PMID29396474
PMCPMC5833686
OpenAlexW2789245860

What OpenQuestion holds

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LicenceCC BY
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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.