Evidence map›Paper›PMID 28740138›Full record

ArticleScientific reports2017

Alantolactone induces apoptosis, promotes STAT3 glutathionylation and enhances chemosensitivity of A549 lung adenocarcinoma cells to doxorubicin via oxidative stress.

Amara Maryam, Tahir Mehmood, He Zhang, Yongming Li, Muhammad Khan, Tonghui Ma

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.1field-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

45 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Role of oxeiptosis in disease mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2025
    Review
  5. Exploring the CaToxicology research · 2025
    Article
  6. Article
  7. Unraveling the complexity of STAT3 in cancer: molecular understanding and drug discovery.Journal of experimental & clinical cancer research : CR · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. PRMT5 Enables Robust STAT3 Activation via Arginine Symmetric Dimethylation of SMAD7.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  20. 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

6 authors at 1 institution in 1 country.

Amara MaryamCollege of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.
Tahir MehmoodCollege of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.
He ZhangCollege of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.
Yongming LiCollege of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China.
Muhammad KhanCollege of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China. khan_zoologist@ymail.com.
Tonghui MaCollege of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning, 116044, People's Republic of China. tonghuima@dlmedu.edu.cn.
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alantolactone (ALT), a sesquiterpene lactone component of Inula helenium, has been reported to exert anticancer activity in various cancers. However, the cellular targets and underlying mechanism of anticancer activity of ALT in various cancers including lung cancer has not been fully defined. In the present study, we found that ALT effectively inhibits proliferation and triggers oxidative stress mediated-apoptosis in A549 lung adenocarcinoma cells by inducing ER stress and mitochondrial dysfunction. This ALT-mediated apoptosis was inhibited by NAC while diamide potentiated it. Moreover, ALT effectively suppressed both constitutive and inducible STAT3 activation, inhibited its translocation into nucleus and decreased its DNA binding activity. Further mechanistic study revealed that ALT abrogated STAT3 activation by promoting STAT3 glutathionylation. ROS scavenger NAC reverted ALT-mediated STAT3 glutathionylation and inhibition of STAT3 phosphorylation. Finally, ALT enhanced chemosensitivity of A549 cells to doxorubicin and reversed doxorubicin resistance in A549/DR cells by inhibiting STAT3 activation and P-glycoprotein expression and increasing intracellular accumulation of doxorubicin. Suppression of STAT3 activation by targeting ROS metabolism with ALT thus discloses a previously unrecognized mechanism underlying the biological activity of ALT. Taken together; ALT induces oxidative stress-dependent apoptosis, inhibits STAT3 activation and augments doxorubicin toxicity in A549 lung cancer cells. These findings provide an in-depth insight into the molecular mechanism of ALT in the treatment of lung cancer.

Indexed as

AdenocarcinomaAntibiotics, AntineoplasticApoptosisCell MovementCell ProliferationDoxorubicinDrug Resistance, NeoplasmGlutathioneHumansLactonesLung NeoplasmsOxidative StressPhosphorylationSesquiterpenes, EudesmaneSTAT3 Transcription FactorTumor Cells, CulturedalantolactoneAntibiotics, AntineoplasticDoxorubicinGlutathioneLactonesSesquiterpenes, EudesmaneSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID28740138
PMCPMC5524969
OpenAlexW2737560814

What OpenQuestion holds

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LicenceCC BY
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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.