Evidence map›Paper›PMID 33994369›Full record

ArticleCancer genomics & proteomics

Cisplatin Activates the Growth Inhibitory Signaling Pathways by Enhancing the Production of Reactive Oxygen Species in Non-small Cell Lung Cancer Carrying an EGFR Exon 19 Deletion.

Md Mohiuddin, Kazuo Kasahara

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

11 citing papers in PubMed, 13 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

2 authors at 1 institution in 1 country.

Md MohiuddinDepartment of Respiratory Medicine, Kanazawa University, Ishikawa, Japan mohiuddin@med.kanazawau.ac.jp.
Kazuo KasaharaDepartment of Respiratory Medicine, Kanazawa University, Ishikawa, Japan.
Kanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimCisplatin is a potent anticancer drug for treating several types of cancer, including non-small-cell lung cancer (NSCLC). In this study, we investigated the cytotoxicity and mechanism of action of cisplatin in the human NSCLC cell line PC9. MATERIALS AND

methodsPC9 cells were treated with cisplatin for 72 h and then evaluated by a cell viability assay, DAPI staining, Giemsa staining, apoptosis assay, membrane permeability assay, cell cycle assay, ROS assay, SA-β-gal staining, TUNEL assay and Western blotting.

resultsOur findings revealed that the cytotoxic activity was associated with an apoptotic signaling pathway in response to DNA damage. Cisplatin exerted a significant concentration-dependent antiproliferative effect on PC9 cells. Cells subjected to cisplatin treatment showed morphological indications of apoptosis. Cell cycle arrest was related to the restriction of E2F-1 action by the cyclin-dependent protein kinase inhibitor p21

conclusionCisplatin induced anticancer effects through cell cycle arrest, ROS generation and caspase activation, resulting in cell apoptosis. Overall, the results show the mechanism by which cisplatin works as an anticancer drug in the treatment of NSCLC.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorCisplatinErbB ReceptorsExonsHumansLung NeoplasmsReactive Oxygen SpeciesSignal TransductionAntineoplastic AgentsCisplatinErbB ReceptorsReactive Oxygen SpeciesapoptosisATRcell cycle arrestCisplatinNSCLCROS

Identifiers

PMID33994369
PMCPMC8240041
OpenAlexW3161017145

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.