Evidence map›Paper›PMID 39034729›Full record

ArticleAnti-cancer agents in medicinal chemistry2024

A Novel Tryptanthrin Derivative D6 Induces Apoptosis and DNA Damage in Non-small-cell Lung Cancer Cells Through Regulating the EGFR Pathway.

Haitao Long, Guanglong Zhang, Yue Zhou, Liqing Qin, Danxue Zhu, Jiayi Chen, Bo Liu, Huayuan Tan, Danping Chen, Zhurui Li and 2 more

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Article in Anti-cancer agents in medicinal chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Chemistry and Biological Activity of 11Molecules (Basel, Switzerland) · 2026
    Review
  2. Medicinal chemistry (Shariqah (United Arab Emirates)) · 2025
    Article
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

12 authors.

Haitao LongSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Guanglong ZhangSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Yue ZhouSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Liqing QinSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Danxue ZhuSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Jiayi ChenSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Bo LiuSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Huayuan TanSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Danping ChenSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Zhurui LiSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Chengpeng LiSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.
Zhenchao WangSchool of Pharmaceutical Sciences, Guizhou University, Guiyang, 550025, China.ORCID 0000-0003-1859-0128

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small-cell lung cancer is a prevalent malignancy associated with significant morbidity and mortality rates. Tryptanthrin and its derivatives have exhibited potent antitumor activity.

objectiveThis study aims to investigate the inhibitory effect of a novel synthesized tryptanthrin derivative D6 on proliferation and the possible mechanism of human non-small cell lung cancer cell lines (A549)

methodsIn this study, MTT assay, cell migration, colony formation assay, cell cycle analysis, cell apoptosis, JC- 1 staining assay, reactive oxygen species analysis, proteomics, western blotting, high content screening and absorption titrations analysis were performed.

resultsWe found that D6 inhibited both the proliferation and migration, induced cell cycle arrest in the G2/M phase, increased levels of ROS, decreased mitochondrial membrane potential, and promoted apoptosis in A549 cells. Further mechanistic studies found that D6 reduced EGFR expression in A549 cells and inhibited the EGFR pathway by decreasing phosphorylation levels of EGFR, Stat3, AKT and Erk1/2. Moreover, DNA damage induced by D6 involved an increase in p53/MDM2 ratio and concentration-dependent accumulation of micronuclei.

conclusionD6 demonstrated significant antitumor activity against A549 cells by inhibiting the EGFR signaling pathway, inducing DNA damage, and subsequently leading to oxidative stress, apoptosis, and cell cycle arrest. Our findings suggest that D6 exhibits potential as an NSCLC drug, owing to its attributes such as antiproliferative activity and ability to induce apoptosis by attenuating the EGFR-mediated signaling pathway.

Indexed as

Antineoplastic AgentsApoptosisCarcinoma, Non-Small-Cell LungCell ProliferationDNA DamageDose-Response Relationship, DrugDrug Screening Assays, AntitumorErbB ReceptorsLung NeoplasmsQuinazolinesHumansMolecular StructureStructure-Activity RelationshipTumor Cells, CulturedAntineoplastic AgentsEGFR protein, humanErbB ReceptorsQuinazolinestryptanthrineanti-cancerapoptosisEGFR.Non-small cell lung cancerproteomicstryptanthrin derivatives

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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.