Evidence map›Paper›PMID 26661339›Full record

ArticleBritish journal of pharmacology2016

Decursin enhances TRAIL-induced apoptosis through oxidative stress mediated- endoplasmic reticulum stress signalling in non-small cell lung cancers.

Jaekwang Kim, Miyong Yun, Eun-Ok Kim, Deok-Beom Jung, Gunho Won, Bonglee Kim, Ji Hoon Jung, Sung-Hoon Kim

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

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  16. Stimulation of ROS Generation by Extract ofAntioxidants (Basel, Switzerland) · 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

8 authors at 1 institution in 1 country.

Jaekwang KimCollege of Korean Medicine, Kyung Hee University, Seoul, South Korea.
Miyong YunCollege of Korean Medicine, Kyung Hee University, Seoul, South Korea.
Eun-Ok KimCollege of Korean Medicine, Kyung Hee University, Seoul, South Korea.
Deok-Beom JungCollege of Korean Medicine, Kyung Hee University, Seoul, South Korea.
Gunho WonCollege of Korean Medicine, Kyung Hee University, Seoul, South Korea.
Bonglee KimCollege of Korean Medicine, Kyung Hee University, Seoul, South Korea.
Ji Hoon JungCollege of Korean Medicine, Kyung Hee University, Seoul, South Korea.
Sung-Hoon KimCollege of Korean Medicine, Kyung Hee University, Seoul, South Korea.
Kyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe TNF-related apoptosis-inducing ligand (TRAIL) is a promising anticancer agent due to its remarkable ability to selectively kill tumour cells. However, because most tumours exhibit resistance to TRAIL-induced apoptosis, the development of combination therapies to overcome resistance to TRAIL is required for effective cancer therapy. EXPERIMENTAL APPROACH: Cell viability and possible synergy between the plant pyranocoumarin decursin and TRAIL was measured by MTT assay and calcusyn software. Reactive oxygen species (ROS) and apoptosis were measured using dichlorodihydrofluorescein and annexin/propidium iodide in cell flow cytometry. Changes in protein levels were assessed with Western blotting. KEY

resultsCombining decursin and TRAIL markedly decreased cell viability and increased apoptosis in TRAIL-resistant non-small-cell lung cancer (NSCLC) cell lines. Decursin induced expression of the death receptor 5 (DR5). Inhibition of DR5 attenuated apoptotic cell death in decursin + TRAIL treated NSCLC cell lines. Interestingly, induction of DR5 and CCAAT/enhancer-binding protein homologues protein by decursin was mediated through selective induction of the pancreatic endoplasmic reticulum kinase (PERK)/activating transcription factor 4 (ATF4) branch of the endoplasmic reticulum stress response pathway. Furthermore, enhancement of PERK/ATF4 signalling by decursin was mediated by ROS generation in NSCLC cell lines, but not in normal human lung cells. Decursin also markedly down-regulated expression of survivin and Bcl-xL in TRAIL-resistant NSCLC cells. CONCLUSIONS AND IMPLICATIONS: ROS generation by decursin selectively activated the PERK/ATF4 axis of the endoplasmic reticulum stress signalling pathway, leading to enhanced TRAIL sensitivity in TRAIL-resistant NSCLC cell lines, partly via up-regulation of DR5.

Indexed as

Activating Transcription Factor 4Antineoplastic AgentsApoptosisBenzopyransButyratesCarcinoma, Non-Small-Cell LungCell LineCell Line, TumorCell SurvivalDrug SynergismeIF-2 KinaseEndoplasmic Reticulum StressHumansLung NeoplasmsOxidative StressReceptors, TNF-Related Apoptosis-Inducing LigandActivating Transcription Factor 4Antineoplastic AgentsATF4 protein, humanBenzopyransButyratesdecursinEIF2AK3 protein, humaneIF-2 KinaseReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandTNFRSF10B protein, human

Identifiers

PMID26661339
PMCPMC5341238
OpenAlexW2275518486

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.