Evidence map›Paper›PMID 36466092›Full record

ArticleOxidative medicine and cellular longevity2022

Modulation of the p38 MAPK Pathway by Anisomycin Promotes Ferroptosis of Hepatocellular Carcinoma through Phosphorylation of H3S10.

Wei Chen, Wenjing Yang, Chunyan Zhang, Te Liu, Jie Zhu, Hao Wang, Tong Li, Anli Jin, Lin Ding, Jingrong Xian and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  7. Review
  8. Article
  9. Targeting the MAPK Pathway in Cancer.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Epigenetic regulation of ferroptosis in gastrointestinal cancers (Review).International journal of molecular medicine · 2025
    Review
  16. Article
  17. Review
  18. Article
  19. Article
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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

14 authors at 1 institution in 1 country.

Wei ChenDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-1651-2046
Wenjing YangDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-0979-0443
Chunyan ZhangDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-0345-6236
Te LiuDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-3976-3489
Jie ZhuDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-0107-3266
Hao WangDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0001-6881-9977
Tong LiDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0001-8343-0046
Anli JinDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-2420-5919
Lin DingDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0001-8207-8693
Jingrong XianDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-6643-3752
Tongtong TianDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-1470-2962
Baishen PanDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Wei GuoDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-9924-638X
Beili WangDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0001-5167-170X
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a prevalent malignant tumor worldwide. Ferroptosis is emerging as an effective target for tumor treatment as it has been shown to potentiate cell death in some malignancies. However, it remains unclear whether histone phosphorylation events, an epigenetic mechanism that regulates transcriptional expression, are involved in ferroptosis. Our study found that supplementation with anisomycin, an agonist of p38 mitogen-activated protein kinase (MAPK), induced ferroptosis in HCC cells, and the phosphorylation of histone H3 on serine 10 (p-H3S10) was participated in anisomycin-induced ferroptosis. To investigate the anticancer effects of anisomycin-activated p38 MAPK in HCC, we analyzed cell viability, colony formation, cell death, and cell migration in Hep3B and HCCLM3 cells. The results showed that anisomycin could significantly suppress HCC cell colony formation and migration and induce HCC cell death. The hallmarks of ferroptosis, such as abnormal accumulation of iron and elevated levels of lipid peroxidation and malondialdehyde, were detected to confirm the ability of anisomycin to promote ferroptosis. Furthermore, coincubation with SB203580, an inhibitor of activated p38 MAPK, partially rescued anisomycin-induced ferroptosis. And the levels of p-p38 MAPK and p-H3S10 were successively increased by anisomycin treatment. The relationship between p-H3S10 and ferroptosis was revealed by ChIP sequencing. The reverse transcription PCR and immunofluorescence results showed that NCOA4 was upregulated both in mRNA and protein levels after anisomycin treatment. And by C11-BODIPY staining, we found that anisomycin-induced lipid reactive oxygen species was reduced after NCOA4 knockdown. In conclusion, the anisomycin-activated p38 MAPK promoted ferroptosis of HCC cells through H3S10 phosphorylation.

Indexed as

Carcinoma, HepatocellularFerroptosisLiver NeoplasmsAnisomycinHistonesHumansp38 Mitogen-Activated Protein KinasesPhosphorylationSerineTranscription FactorsAnisomycinHistonesp38 Mitogen-Activated Protein KinasesSerineTranscription Factors

Identifiers

PMID36466092
PMCPMC9715334
OpenAlexW4309905693

What OpenQuestion holds

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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 OpenQuestion graph.