Evidence map›Paper›PMID 24905917›Full record

ArticleAutophagy2014

Activation of the MAPK11/12/13/14 (p38 MAPK) pathway regulates the transcription of autophagy genes in response to oxidative stress induced by a novel copper complex in HeLa cells.

Wu Zhong, Haichuan Zhu, Fugeng Sheng, Yonglu Tian, Jun Zhou, Yingyu Chen, Song Li, Jian Lin

Abstract read
In one paragraph

Article in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing 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

65 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Disruption of Copper Redox Balance and Dysfunction underEnvironment & health (Washington, D.C.) · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Synergistic Effect of SiONanomaterials (Basel, Switzerland) · 2024
    Article
  14. Article
  15. Life science alliance · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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.

Wu ZhongLaboratory of Computer-Aided Drug Design and Discovery; Beijing Institute of Pharmacology and Toxicology; Beijing, China.
Haichuan ZhuLaboratory of Computer-Aided Drug Design and Discovery; Beijing Institute of Pharmacology and Toxicology; Beijing, China; Synthetic and Functional Biomolecules Center; College of Chemistry and Molecular Engineering; Peking University; Beijing, China.
Fugeng ShengDepartment of Radiology; Affiliated Hospital of the Academy of Military Medical Science; Beijing, China.
Yonglu TianLaboratory Animal Centre; Peking University; Beijing, China.
Jun ZhouLaboratory of Computer-Aided Drug Design and Discovery; Beijing Institute of Pharmacology and Toxicology; Beijing, China.
Yingyu ChenCentre for Human Disease Genomics; Peking University; Beijing, China.
Song LiLaboratory of Computer-Aided Drug Design and Discovery; Beijing Institute of Pharmacology and Toxicology; Beijing, China.
Jian LinSynthetic and Functional Biomolecules Center; College of Chemistry and Molecular Engineering; Peking University; Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transition metal copper (Cu) can exist in oxidized or reduced states in cells, leading to cytotoxicity in cancer cells through oxidative stress. Recently, copper complexes are emerging as a new class of anticancer compounds. Here, we report that a novel anticancer copper complex (HYF127c/Cu) induces oxidative stress-dependent cell death in cancer cells. Further, transcriptional analysis revealed that oxidative stress elicits broad transcriptional changes of genes, in which autophagy-related genes are significantly changed in HYF127c/Cu-treated cells. Consistently, autophagy was induced in HYF127c/Cu-treated cells and inhibitors of autophagy promoted cell death induced by HYF127c/Cu. Further analysis identified that the MAPK11/12/13/14 (formerly known as p38 MAPK) pathway was also activated in HYF127c/Cu-treated cells. Meanwhile, the MAPK11/12/13/14 inhibitor SB203580 downregulated autophagy by inhibiting the transcription of the autophagy genes MAP1LC3B, BAG3, and HSPA1A, and promoted HYF127c/Cu-induced cell death. These data suggest that copper-induced oxidative stress will induce protective autophagy through transcriptional regulation of autophagy genes by activation of the MAPK11/12/13/14 pathway in HeLa cells.

Indexed as

ApoptosisAutophagyCell ProliferationCopperDown-RegulationEnzyme ActivationGene Expression Regulation, NeoplasticHeLa CellsHumansImidazolesMAP Kinase Signaling SystemNeoplasm ProteinsNeoplasmsOxidative Stressp38 Mitogen-Activated Protein KinasesPyridinesCopperImidazolesNeoplasm Proteinsp38 Mitogen-Activated Protein KinasesPyridinesSB 203580autophagycopperHYF127c/CuMAPK11MAPK12MAPK13MAPK14oxidative stressp38 mitogen-activated protein kinasetranscription

Identifiers

PMID24905917
PMCPMC4203553

What OpenQuestion holds

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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.