Evidence map›Paper›PMID 24832602›Full record

ArticleCell death & disease2014

β-Lapachone induces programmed necrosis through the RIP1-PARP-AIF-dependent pathway in human hepatocellular carcinoma SK-Hep1 cells.

E J Park, K-J Min, T-J Lee, Y H Yoo, Y-S Kim, T K Kwon

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
8.3field-weighted citation impact, top 1% 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

61 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. International journal of molecular sciences · 2023
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

1 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

6 authors at 4 institutions in 1 country.

E J ParkDepartment of Immunology, School of Medicine, Keimyung University, Daegu, Korea.
K-J MinDepartment of Immunology, School of Medicine, Keimyung University, Daegu, Korea.
T-J LeeDepartment of Anatomy, College of Medicine, Yeungnam University, Daegu, Korea.
Y H YooDepartment of Anatomy and Cell Biology and Mitochondria Hub Regulation Center, Dong-A University College of Medicine, Busan, Korea.
Y-S KimDepartment of Biochemistry, Ajou University School of Medicine, San 5, Wonchon-dong, Yeongtong-gu, Suwon, Korea.
T K KwonDepartment of Immunology, School of Medicine, Keimyung University, Daegu, Korea.
Keimyung University · KRAjou University · KRDong-A University · KRYeungnam University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-Lapachone activates multiple cell death mechanisms including apoptosis, autophagy and necrotic cell death in cancer cells. In this study, we investigated β-lapachone-induced cell death and the underlying mechanisms in human hepatocellular carcinoma SK-Hep1 cells. β-Lapachone markedly induced cell death without caspase activation. β-Lapachone increased PI uptake and HMGB-1 release to extracellular space, which are markers of necrotic cell death. Necrostatin-1 (a RIP1 kinase inhibitor) markedly inhibited β-lapachone-induced cell death and HMGB-1 release. In addition, β-lapachone activated poly (ADP-ribosyl) polymerase-1(PARP-1) and promoted AIF release, and DPQ (a PARP-1 specific inhibitor) or AIF siRNA blocked β-lapachone-induced cell death. Furthermore, necrostatin-1 blocked PARP-1 activation and cytosolic AIF translocation. We also found that β-lapachone-induced reactive oxygen species (ROS) production has an important role in the activation of the RIP1-PARP1-AIF pathway. Finally, β-lapachone-induced cell death was inhibited by dicoumarol (a NQO-1 inhibitor), and NQO1 expression was correlated with sensitivity to β-lapachone. Taken together, our results demonstrate that β-lapachone induces programmed necrosis through the NQO1-dependent ROS-mediated RIP1-PARP1-AIF pathway.

Indexed as

Antineoplastic AgentsApoptosis Inducing FactorCarcinoma, HepatocellularCell Line, TumorDose-Response Relationship, DrugHMGB1 ProteinHumansLiver NeoplasmsNAD(P)H Dehydrogenase (Quinone)NaphthoquinonesNecrosisNuclear Pore Complex ProteinsPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesProtein Kinase InhibitorsAGFG1 protein, humanAIFM1 protein, humanAntineoplastic AgentsApoptosis Inducing Factorbeta-lapachoneHMGB1 ProteinHMGB1 protein, humanNAD(P)H Dehydrogenase (Quinone)NaphthoquinonesNQO1 protein, humanNuclear Pore Complex ProteinsPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesProtein Kinase InhibitorsReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRNA-Binding Proteins

Identifiers

PMID24832602
PMCPMC4047891
OpenAlexW2043947838

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.