Evidence map›Paper›PMID 25009698›Full record

ArticleBiomolecules & therapeutics2014

β-lapachone-Induced Apoptosis of Human Gastric Carcinoma AGS Cells Is Caspase-Dependent and Regulated by the PI3K/Akt Pathway.

Hai Yang Yu, Sung Ok Kim, Cheng-Yun Jin, Gi-Young Kim, Wun-Jae Kim, Young Hyun Yoo, Yung Hyun Choi

Abstract read
In one paragraph

Article in Biomolecules & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  4. International journal of molecular sciences · 2023
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  5. Review
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  7. Review
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  14. Article
  15. Enhancing Oral Absorption of β-Lapachone: Progress Till Date.European journal of drug metabolism and pharmacokinetics · 2017
    Review
  16. Article
  17. Article
  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

7 authors at 6 institutions in 2 countries.

Hai Yang YuCollege of Natural Resources and Life Science, Dong-A University, Busan 604-714.
Sung Ok KimTeam for Scientification of Korean Medical Intervention (BK21 Plus) & Department of Herbal Pharmacology, College of Oriental Medicine, Daegu Haany University, Daegu 706-828.
Cheng-Yun JinSchool of Pharmaceutical Science, Zhengzhou University, Henan 450001, China.
Gi-Young KimLaboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Jeju 690-756.
Wun-Jae KimDepartment of Urology, Chungbuk National University College of Medicine, Cheongju 361-804.
Young Hyun YooDepartment of Anatomy and Cell Biology, Dong-A University College of Medicine and Mitochondria Hub Regulation Center, Busan 602-714.
Yung Hyun ChoiDepartment of Biochemistry, Dongeui University College of Oriental Medicine, Busan 614-052 ; Anti-Aging Research Center & Blue-Bio Industry RIC, Dongeui University, Busan 614-714, Republic of Korea.
Dong-A University · KRChungbuk National University · KRDaegu Haany University · KRDong-Eui University · KRJeju National University · KRZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-lapachone is a naturally occurring quinone that selectively induces apoptotic cell death in a variety of human cancer cells in vitro and in vivo; however, its mechanism of action needs to be further elaborated. In this study, we investigated the effects of β-lapachone on the induction of apoptosis in human gastric carcinoma AGS cells. β-lapachone significantly inhibited cellular proliferation, and some typical apoptotic characteristics such as chromatin condensation and an increase in the population of sub-G1 hypodiploid cells were observed in β-lapachone-treated AGS cells. Treatment with β-lapachone caused mitochondrial transmembrane potential dissipation, stimulated the mitochondria-mediated intrinsic apoptotic pathway, as indicated by caspase-9 activation, cytochrome c release, Bcl-2 downregulation and Bax upregulation, as well as death receptor-mediated extrinsic apoptotic pathway, as indicated by activation of caspase-8 and truncation of Bid. This process was accompanied by activation of caspase-3 and concomitant with cleavage of poly(ADP-ribose) polymerase. The general caspase inhibitor, z-VAD-fmk, significantly abolished β-lapachone-induced cell death and inhibited growth. Further analysis demonstrated that the induction of apoptosis by β-lapachone was accompanied by inactivation of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. The PI3K inhibitor LY29004 significantly increased β-lapachone-induced apoptosis and growth inhibition. Taken together, these findings indicate that the apoptotic activity of β-lapachone is probably regulated by a caspase-dependent cascade through activation of both intrinsic and extrinsic signaling pathways, and that inhibition of the PI3K/Akt signaling may contribute to β-lapachone-mediated AGS cell growth inhibition and apoptosis induction.

Indexed as

ApoptosisCaspasePI3K/Aktβ-lapachone

Identifiers

PMID25009698
PMCPMC4060078
OpenAlexW2075111099

What OpenQuestion holds

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LicenceCC BY-NC
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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.