Evidence map›Paper›PMID 30406888›Full record

ArticleMolecular biology reports2018

Diclofenac induced apoptosis via altering PI3K/Akt/MAPK signaling axis in HCT 116 more efficiently compared to SW480 colon cancer cells.

Elif Damla Arisan, Zehragül Ergül, Gülnihal Bozdağ, Özge Rencüzoğulları, Ajda Çoker-Gürkan, Pınar Obakan-Yerlikaya, Deniz Coşkun, Narçin Palavan-Ünsal

Abstract read
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In one paragraph

Article in Molecular biology reports, 2018. 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
2.9field-weighted citation impact, top 9% 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, 32 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

8 authors at 1 institution in 1 country.

Elif Damla ArisanScience and Literature Faculty, Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, 34156, Istanbul, Turkey. d.arisan@iku.edu.tr.ORCID http://orcid.org/0000-0002-4844-6381
Zehragül ErgülScience and Literature Faculty, Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, 34156, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-1466-5068
Gülnihal BozdağScience and Literature Faculty, Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, 34156, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-1275-1720
Özge RencüzoğullarıScience and Literature Faculty, Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, 34156, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-2157-1289
Ajda Çoker-GürkanScience and Literature Faculty, Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, 34156, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-1475-2417
Pınar Obakan-YerlikayaScience and Literature Faculty, Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, 34156, Istanbul, Turkey.ORCID http://orcid.org/0000-0001-7058-955X
Deniz CoşkunScience and Literature Faculty, Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, 34156, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-7102-3969
Narçin Palavan-ÜnsalScience and Literature Faculty, Department of Molecular Biology and Genetics, Istanbul Kultur University, Atakoy Campus, 34156, Istanbul, Turkey.ORCID http://orcid.org/0000-0001-6366-6908
Istanbul Kültür University · TR

Funding

Türkiye Bilimsel ve Teknolojik Araştirma Kurumu 2209
6 · The paper itself

Abstract

Diclofenac is a preferential cyclooxygenase 2 inhibitor (COX-2) and member of non-steroidal anti-inflammatory drugs (NSAIDs). Inflammation is one of the main reason of poor prognosis of colon cancer cases; thereby NSAIDs are potential therapeutic agents in colon cancer therapy. In this study, our aim to understand the potential molecular targets of diclofenac, which may propose new therapeutic targets in HCT 116 (wt p53) and SW480 (mutant p53R273H) colon cancer cells. For this purpose, we identified different response against diclofenac treatment through expression profiles of PI3K/Akt/MAPK signaling axis. Our hypothesis was diclofenac-mediated apoptosis is associated with inhibition of PI3K/Akt/MAPK signaling axis. We found that sub-cytotoxic concentration of diclofenac (400 µM) promoted further apoptosis in HCT 116 cells compared to SW480 colon cancer cells. Diclofenac triggered dephosphorylation of PTEN, PDK, Akt, which led to inhibition of PI3K/Akt survival axis in HCT 116 colon cancer cells. However, diclofenac showed lesser effect in SW480 colon cancer cells. In addition, diclofenac further activated p44/42, p38 and SAPK/JNK in HCT 116 cells compared to SW480 cells.

Indexed as

ApoptosisCell Line, TumorCell SurvivalColonColonic NeoplasmsCyclooxygenase 2 InhibitorsDiclofenacHCT116 CellsHumansMAP Kinase Signaling SystemPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseCyclooxygenase 2 InhibitorsDiclofenacPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanApoptosisColon cancerDiclofenacNSAID

Identifiers

PMID30406888
OpenAlexW2899803459

What OpenQuestion holds

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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.