Evidence map›Paper›PMID 30720135›Full record

ArticleInternational journal of oncology2019

A novel mechanism for the anticancer activity of aspirin and salicylates.

Asma'u I J Bashir, Chandra S Kankipati, Sarah Jones, Robert M Newman, Stephen T Safrany, Christopher J Perry, Iain D Nicholl

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-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

20 citing papers in PubMed, 42 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

7 authors at 2 institutions in 2 countries.

Asma'u I J BashirDepartment of Biomedical Science and Physiology, School of Sciences, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton WV1 1LY, UK.
Chandra S KankipatiDepartment of Biomedical Science and Physiology, School of Sciences, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton WV1 1LY, UK.
Sarah JonesSchool of Pharmacy, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton WV1 1LY, UK.
Robert M NewmanSchool of Mathematics and Computer Science, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton WV1 1LY, UK.
Stephen T SafranySchool of Medicine, RCSI‑Bahrain, Adliya, Kingdom of Bahrain.
Christopher J PerrySchool of Pharmacy, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton WV1 1LY, UK.
Iain D NichollDepartment of Biomedical Science and Physiology, School of Sciences, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton WV1 1LY, UK.
University of Wolverhampton · GBRoyal College of Surgeons in Ireland - Bahrain · BH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidemiological studies indicate that long‑term aspirin usage reduces the incidence of colorectal cancer (CRC) and may protect against other non‑CRC associated adenocarcinomas, including oesophageal cancer. A number of hypotheses have been proposed with respect to the molecular action of aspirin and other non‑steroidal anti‑inflammatory drugs in cancer development. The mechanism by which aspirin exhibits toxicity to CRC has been previously investigated by synthesising novel analogues and derivatives of aspirin in an effort to identify functionally significant moieties. Herein, an early effect of aspirin and aspirin‑like analogues against the SW480 CRC cell line was investigated, with a particular focus on critical molecules in the epidermal growth factor (EGF) pathway. The present authors proposed that aspirin, diaspirin and analogues, and diflunisal (a salicylic acid derivative) may rapidly perturb EGF and EGF receptor (EGFR) internalisation. Upon longer incubations, the diaspirins and thioaspirins may inhibit EGFR phosphorylation at Tyr1045 and Tyr1173. It was additionally demonstrated, using a qualitative approach, that EGF internalisation in the SW480 cell line may be directed to endosomes by fumaryldiaspirin using early endosome antigen 1 as an early endosomal marker and that EGF internalisation may also be perturbed in oesophageal cell lines, suggestive of an effect not only restricted to CRC cells. Taken together and in light of our previous findings that the aspirin‑like analogues can affect cyclin D1 expression and nuclear factor‑κB localisation, it was hypothesized that aspirin and aspirin analogues significantly and swiftly perturb the EGFR axis and that the protective activity of aspirin may in part be explained by perturbed EGFR internalisation and activation. These findings may also have implications in understanding the inhibitory effect of aspirin and salicylates on wound healing, given the critical role of EGF in the response to tissue trauma.

Indexed as

AspirinCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsCyclin D1Drug Screening Assays, AntitumorEGF Family of ProteinsErbB ReceptorsGene Expression Regulation, NeoplasticHumansNF-kappa BPhosphorylationSalicylatesSignal TransductionAspirinCCND1 protein, humanCyclin D1EGF Family of ProteinsErbB ReceptorsNF-kappa BSalicylatesaspirincolorectal cancerendocytosisepidermal growth factorepidermal growth factor receptor

Identifiers

PMID30720135
PMCPMC6411351
OpenAlexW2912297809

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.