Evidence map›Paper›PMID 35813479›Full record

ArticleInternational journal of biological sciences2022

Daidzein Synergizes with Gefitinib to Induce ROS/JNK/c-Jun Activation and Inhibit EGFR-STAT/AKT/ERK Pathways to enhance Lung Adenocarcinoma cells chemosensitivity.

Thomas Gabriel Mhone, Ming-Cheng Chen, Chia-Hua Kuo, Tzu-Ching Shih, Chung-Min Yeh, Tso-Fu Wang, Ray-Jade Chen, Yu-Chun Chang, Wei-Wen Kuo, Chih-Yang Huang

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 45 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

10 authors at 7 institutions in 1 country.

Thomas Gabriel MhoneGraduate Institute of Biomedical Sciences, China Medical University, Taichung 404, Taiwan.
Ming-Cheng ChenDivision of Colorectal Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung 40705, Taiwan.
Chia-Hua KuoLaboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Tzu-Ching ShihDepartment of Biomedical Imaging & Radiological Science College of Medicine, China Medical University, Taichung 404, Taiwan.
Chung-Min YehDepartment of Pathology, Changhua Christian Hospital, Changhua 500, Taiwan.
Tso-Fu WangDepartment of Hematology and Oncology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
Ray-Jade ChenDepartment of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Yu-Chun ChangCardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
Wei-Wen KuoDepartment of Biological Science and Technology, China Medical University, Taichung 406, Taiwan.
Chih-Yang HuangGraduate Institute of Biomedical Sciences, China Medical University, Taichung 404, Taiwan.
China Medical University · TWTzu Chi Foundation · TWChanghua Christian Hospital · TWNational Yang Ming University Hospital · TWTaipei Medical University · TWTzu Chi University · TWUniversity of Taipei · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the major cause of cancer associated mortality. Mutations in EGFR have been implicated in lung cancer pathogenesis. Gefitinib (GF) is a RTKI (receptor tyrosine kinase inhibitor) first-choice drug for EGFR mutated advanced lung cancer. However, drug toxicity and cancer cell resistance lead to treatment failure. Consequently, new therapeutic strategies are urgently required. Therefore, this study was aimed at identifying tumor suppressive compounds that can synergistically improve Gefitinib chemosensitivity in the lung cancer treatment. Medicinal plants offer a vast platform for the development of novel anticancer agents. Daidzein (DZ) is an isoflavone compound extracted from soy plants and has been shown to possess many medicinal benefits. The anticancer potential of GF and DZ combination treatment was investigated using MTT, western blot, fluorescent microscopy imaging, flow cytometry and nude mice tumor xenograft techniques. Our results demonstrate that DZ synergistically induces c-Jun nuclear translocation through ROS/ASK1/JNK and downregulates EGFR-STAT/AKT/ERK pathways to activate apoptosis and a G0/G1 phase cell cycle blockade. In in-vivo, the combination treatment significantly suppressed A549 lung cancer cells tumor xenograft growth without noticeable toxicity. Daidzein supplements with current chemotherapeutic agents may well be an alternative strategy to improve the treatment efficacy of lung adenocarcinoma.

Indexed as

Adenocarcinoma of LungAntineoplastic AgentsIsoflavonesLung NeoplasmsAnimalsApoptosisCell Line, TumorDrug Resistance, NeoplasmErbB ReceptorsGefitinibHumansMAP Kinase Signaling SystemMiceMice, NudeProto-Oncogene Proteins c-aktReactive Oxygen SpeciesAntineoplastic AgentsdaidzeinEGFR protein, humanErbB ReceptorsGefitinibIsoflavonesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesApoptosisChemosensitivityc-JunDaidzeinROSSynergistic

Identifiers

PMID35813479
PMCPMC9254481
OpenAlexW4285028383

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.