Evidence map›Paper›PMID 24763055›Full record

ArticleCell death & disease2014

Therapeutic ROS targeting of GADD45γ in the induction of G2/M arrest in primary human colorectal cancer cell lines by cucurbitacin E.

Y-C Hsu, T-Y Huang, M-J Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Roles for GADD45 in Development and Cancer.Advances in experimental medicine and biology · 2022
    Review
  5. Use of cucurbitacins for lung cancer research and therapy.Cancer chemotherapy and pharmacology · 2021
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Targeting Reactive Oxygen Species in Cancer via Chinese Herbal Medicine.Oxidative medicine and cellular longevity · 2019
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 3 institutions in 1 country.

Y-C Hsu1] Graduate Institute of Medical Science, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan [2] Innovative Research Center of Medicine, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan.
T-Y HuangDepartment of Neurosurgery, Tainan Sin-Lau Hospital, Tainan, Taiwan.
M-J Chen1] Division of Traumatology, Department of Surgery, Chi Mei Medical Center, Tainan, Taiwan [2] Department of Sports Management, College of Leisure and Recreation Management, Chia Nan University of Pharmacy and Science, Tainan, Taiwan.
Chang Jung Christian University · TWChi Mei Medical Center · TWSin-Lau Christian Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cucurbitacin E (CuE) or α-elaterin is a natural compound previously shown to be an antifeedant as well as a potent chemopreventive agent against several types of cancer. The present study investigated the anticancer effects of CuE on colorectal cancer (CRC) using primary cell lines isolated from five CRC patients in Taiwan, Specifically, we explored the anti-proliferation and cell cycle G2/M arrest induced by CuE in CRC cells. MPM-2 flow cytometry tests show that CuE-treated cells accumulated in metaphase (CuE 2.5-7.5 μM). Results further indicate that CuE produced G2/M arrest as well as the downregulation of CDC2 and cyclin B1 expression and dissociation. Both effects increased proportionally with the dose of CuE; however, the inhibition of proliferation, arrest of mitosis, production of reactive oxygen species (ROS), and loss of mitochondrial membrane potential (ΔΨm) were found to be dependent on the quantity of CuE used to treat the cancer cells. In addition, cell cycle arrest in treated cells coincided with the activation of the gene GADD45(α, β, γ). Incubation with CuE resulted in the binding of GADD45γ to CDC2, which suggests that the delay in CuE-induced mitosis is regulated by the overexpression of GADD45γ. Our findings suggest that, in addition to the known effects on cancer prevention, CuE may have antitumor activities in established CRC.

Indexed as

ApoptosisCDC2 Protein KinaseCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsCyclin B1Cyclin-Dependent KinasesDown-RegulationG2 Phase Cell Cycle CheckpointsGADD45 ProteinsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMitosisCDC2 Protein KinaseCDK1 protein, humancucurbitacin ECyclin B1Cyclin-Dependent KinasesGADD45 ProteinsIntracellular Signaling Peptides and ProteinsReactive Oxygen SpeciesTriterpenes

Identifiers

PMID24763055
PMCPMC4001305
OpenAlexW2040265901

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.