Evidence map›Paper›PMID 23717422›Full record

ArticlePloS one2013

Apoptosis induction of human bladder cancer cells by sanguinarine through reactive oxygen species-mediated up-regulation of early growth response gene-1.

Min Ho Han, Cheol Park, Cheng-Yun Jin, Gi-Young Kim, Young-Chae Chang, Sung-Kwon Moon, Wun-Jae Kim, Yung Hyun Choi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 54 citations in OpenAlex.

  1. Sanguinarine Induces HBiomedicines · 2022
    Article
  2. Role of the JNK Pathway in Bladder Cancer.OncoTargets and therapy · 2022
    Review
  3. Antibacterial Therapy by AgInternational journal of molecular sciences · 2021
    Article
  4. Article
  5. Current updates on the role of reactive oxygen species in bladder cancer pathogenesis and therapeutics.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Review
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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

8 authors at 6 institutions in 2 countries.

Min Ho HanAnti-Aging Research Center & Blue-Bio Industry RIC, Dongeui University, Busan, Republic of Korea.
Cheol Park
Cheng-Yun Jin
Gi-Young Kim
Young-Chae Chang
Sung-Kwon Moon
Wun-Jae Kim
Yung Hyun Choi
Dong-Eui University · KRCatholic University of Daegu · KRChung-Ang University · KRChungbuk National University · KRJeju National University · KRZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the effects of sanguinarine, a benzophenanthridine alkaloid, on the inhibition of some kinds of cancer cell growth have been established, the underlying mechanisms are not completely understood. This study investigated possible mechanisms by which sanguinarine exerts its anticancer action in cultured human bladder cancer cell lines (T24, EJ, and 5637). Sanguinarine treatment resulted in concentration-response growth inhibition of the bladder cancer cells by inducing apoptosis. Sanguinarine-induced apoptosis was correlated with the up-regulation of Bax, the down-regulation of Bid and XIAP, the activation of caspases (-3, -8, and -9), and the generation of increased reactive oxygen species (ROS). The ROS scavenger N-acetyl cysteine (NAC) completely reversed the sanguinarine-triggered apoptotic events. In addition, sanguinarine effectively increased the activation of the c-Jun N-terminal kinase (JNK) and the expression of the early growth response gene-1 (Egr-1), which was recovered by pretreatment with NAC. Furthermore, knockdown of Egr-1 expression by small interfering RNA attenuated sanguinarine-induced apoptosis, but not the JNK inhibitor, indicating that the interception of ROS generation blocked the sanguinarine-induced apoptotic effects via deregulation of the expression of Egr-1 proteins. Taken together, the data provide evidence that sanguinarine is a potent anticancer agent, which inhibits the growth of bladder cancer cells and induces their apoptosis through the generation of free radicals.

Indexed as

Antineoplastic AgentsApoptosisbcl-2-Associated X ProteinBenzophenanthridinesBH3 Interacting Domain Death Agonist ProteinCaspasesCell Line, TumorCell SurvivalDown-RegulationEarly Growth Response Protein 1HumansIsoquinolinesJNK Mitogen-Activated Protein KinasesReactive Oxygen SpeciesUp-RegulationUrinary Bladder NeoplasmsAntineoplastic Agentsbcl-2-Associated X ProteinBenzophenanthridinesBH3 Interacting Domain Death Agonist ProteinBID protein, humanCaspasesEarly Growth Response Protein 1EGR1 protein, humanIsoquinolinesJNK Mitogen-Activated Protein KinasesReactive Oxygen SpeciessanguinarineXIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID23717422
PMCPMC3661671
OpenAlexW1966018626

What OpenQuestion holds

Textmetadata
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.