Evidence map›Paper›PMID 39575456›Full record

ArticleInternational journal of oncology2025

Induction of ferroptosis by SIRT1 knockdown alleviates cytarabine resistance in acute myeloid leukemia by activating the HMGB1/ACSL4 pathway.

Qian Kong, Qixiang Liang, Yinli Tan, Xiangqin Luo, Yesheng Ling, Xiaofeng Li, Yun Cai, Huiqin Chen

Abstract read
In one paragraph

Article in International journal of oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Involvement of HMGB1-mediated ferroptosis in systemic diseases.Frontiers in cell and developmental biology · 2025
    Review
  15. The mechanism study of quercetin isolated fromFrontiers in pharmacology · 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

8 authors.

Qian Kong *Department of Pediatrics, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Qixiang Liang *Department of Stomatology, The Third Affiliated Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510000, P.R. China.
Yinli Tan *Department of Pediatrics, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Xiangqin LuoDepartment of Pediatrics, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Yesheng LingDepartment of Pediatrics, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Xiaofeng LiDepartment of Pediatrics, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Yun CaiDepartment of Pediatrics, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Huiqin ChenDepartment of Pediatrics, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance to cytarabine is a major obstacle to the successful treatment of acute myeloid leukemia (AML). The present study aimed to explore the mechanism by which sirtuin 1 (SIRT1) reverses the cytarabine resistance of leukemia cells. Cell viability was investigated using the EdU proliferation assay. The expression levels of molecules were determined by reverse transcription‑quantitative PCR, western blotting, and immunofluorescence staining. Flow cytometry was used to detect reactive oxygen species and apoptosis levels, The levels of superoxide dismutase, glutathione and malondialdehyde were examined by ELISA. Mitochondrial damage was investigated by transmission electron microscopy. Furthermore, tumor growth was evaluated in a xenograft model. The results revealed that SIRT1 expression was significantly upregulated in drug‑resistant leukemia cells. By contrast, knockdown of SIRT1 reversed cytarabine resistance in HL60 cells by promoting ferroptosis. Mechanistically, SIRT1 could regulate the translocation of HMGB1 from the nucleus to the cytoplasm in cytarabine‑resistant HL60 (HL60/C) cells. Furthermore, knockdown of HMGB1 inhibited the expression of ACSL4. In addition, knockdown of SIRT1 expression could inhibit the growth of HL60/C cells

Indexed as

CytarabineDrug Resistance, NeoplasmFerroptosisGene Knockdown TechniquesHMGB1 ProteinLeukemia, Myeloid, AcuteSirtuin 1AnimalsAntimetabolites, AntineoplasticCell ProliferationFemaleHL-60 CellsHumansMaleMiceSignal TransductionAntimetabolites, AntineoplasticCytarabineHMGB1 ProteinHMGB1 protein, humanSIRT1 protein, humanSirtuin 1acute myeloid leukemiaferroptosisHMGB1resistancesirtuin 1

Identifiers

PMID39575456
PMCPMC11637499

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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.