Evidence map›Paper›PMID 24367681›Full record

ArticlePloS one2013

Norcantharidin induced DU145 cell apoptosis through ROS-mediated mitochondrial dysfunction and energy depletion.

Bo Shen, Pei-Jie He, Chun-Lin Shao

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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Pyrazolo[4,3-International journal of molecular sciences · 2023
    Article
  5. Article
  6. Peptide ofFrontiers in cellular and infection microbiology · 2022
    Article
  7. The impact of mitochondria on cancer treatment resistance.Cellular oncology (Dordrecht, Netherlands) · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. ROS in cancer therapy: the bright side of the moon.Experimental & molecular medicine · 2020
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. ROS-modulated therapeutic approaches in cancer treatment.Journal of cancer research and clinical oncology · 2017
    Review
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

3 authors at 1 institution in 1 country.

Bo ShenInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Pei-Jie HeEye, Ear, Nose and Throat Hospital, Fudan University, Shanghai, China.
Chun-Lin ShaoInstitute of Radiation Medicine, Fudan University, Shanghai, China.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Norcantharidin (NCTD), a demethylated analog of cantharidin derived from blister beetles, has attracted considerable attentions in recent years due to their definitely toxic properties and the noteworthy advantages in stimulating bone marrow and increasing the peripheral leukocytes. Hence, it is worth studying the anti-tumor effect of NCTD on human prostate cancer cells DU145. It was found that after the treatment of NCTD with different concentrations (25-100 μM), the cell proliferation was significantly inhibited, which led to the appearance of micronucleus (MN). Moreover, the cells could be killed in a dose-/time-dependent manner along with the reduction of PCNA (proliferating cell nuclear antigen) expression, destruction of mitochondrial membrane potential (MMP), down-regulation of MnSOD, induction of ROS, depletion of ATP, and activation of AMPK (Adenosine 5'-monophosphate -activated protein kinase) . In addition, a remarkable release of cytochrome c was found in the cells exposed to 100 μM NCTD and exogenous SOD-PEG could eliminate the generation of NCTD-induced MN. In conclusion, our studies indicated that NCTD could induce the collapse of MMP and mitochondria dysfunction. Accumulation of intercellular ROS could eventually switch on the apoptotic pathway by causing DNA damage and depleting ATP.

Indexed as

Adenosine TriphosphateAMP-Activated Protein KinasesAntineoplastic AgentsApoptosisBisbenzimidazoleBlotting, WesternBridged Bicyclo Compounds, HeterocyclicCell Line, TumorCell ProliferationCytochromes cDose-Response Relationship, DrugFlow CytometryHumansIn Situ Nick-End LabelingMaleMembrane Potential, MitochondrialAdenosine TriphosphateAMP-Activated Protein KinasesAntineoplastic AgentsBisbenzimidazoleBridged Bicyclo Compounds, HeterocyclicCytochromes cnorcantharidinProliferating Cell Nuclear AntigenReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID24367681
PMCPMC3868658
OpenAlexW2075567933

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.