Evidence map›Paper›PMID 19154411›Full record

ArticleCancer science2009

Formosanin C-induced apoptosis requires activation of caspase-2 and change of mitochondrial membrane potential.

Jenq-Chang Lee, Chun-Li Su, Lin-Lin Chen, Shen-Jeu Won

Abstract read
In one paragraph

Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Formosanin C attenuates lipopolysaccharide-induced inflammation through nuclear factor-κB inhibition in macrophages.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Whole Peptidoglycan Extracts from theBioMed research international · 2018
    Article
  14. Anticancer Effects of Paris Saponins by Apoptosis and PI3K/AKT Pathway in Gefitinib-Resistant Non-Small Cell Lung Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2016
    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

4 authors.

Jenq-Chang LeeDepartment of Surgery, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chun-Li Su
Lin-Lin Chen
Shen-Jeu Won

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Formosanin C is a pure compound isolated from Paris formosana Hayata (Liliaceae). The antitumor efficacy of formosanin C has been observed in cultured cells and animal systems. However, the molecular mechanisms of formosanin C remain unknown. The results of the present study indicate that formosanin C induced apoptosis of HT-29 cells characterized by exposure of phosphatidylserine, accumulation of cells at the sub-G(1) phase, fragmentation of DNA, and change of nuclear morphology in a time- and dose-related manner. The apoptotic signaling cascades may proceed via proteolytic activation of caspase-2, change of mitochondrial membrane potential (Deltapsi(m)), release of cytochrome c and second mitochondria-derived activator of caspase/direct IAP binding protein with low pI (Smac/DIABLO), activation of caspase-9 and -3, and cleavage of poly(ADP-ribose) polymerase (PARP). Increase in apoptosis-inducing factor and endonuclease G expressions in nuclei, and increase in Bax and Bak expressions and decrease in Bcl-X(L) expression on mitochondria were also observed in formosanin C-treated HT-29 cells. Attenuation of formosanin C-induced change of Deltapsi(m) by caspase-2 inhibitor (Z-VDVAC) implies that caspase-2 acts upstream of the mitochondria. Blockage of formosanin C-induced apoptotic process by using either permeability transition pore inhibitor (cyclosporine A) or caspase-9 inhibitor (Z-LEHD) demonstrates the necessity of mitochondria and caspase-9 in formosanin C-induced apoptosis of HT-29 cells. Taken together, the apoptotic mechanism of formosanin C in human colorectal cancer HT-29 cells involves activation of caspase-2 and the dysfunction of mitochondria.

Indexed as

Antineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBlotting, WesternCaspase 2Caspase 3Caspase 9Cell ProliferationCell SurvivalCytochromes cDiosgeninDNA FragmentationEnzyme ActivationHT29 CellsHumansIntracellular Signaling Peptides and ProteinsAntineoplastic AgentsApoptosis Regulatory ProteinsCaspase 2Caspase 3Caspase 9Cytochromes cDIABLO protein, humanDiosgeninformosanin CIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsSaponins

Identifiers

PMID19154411
PMCPMC11159299

What OpenQuestion holds

Textmetadata
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.