Evidence map›Paper›PMID 32872665›Full record

ArticleMolecules (Basel, Switzerland)2020

16-Hydroxycleroda-3,13-dien-15,16-olide Induces Apoptosis in Human Bladder Cancer Cells through Cell Cycle Arrest, Mitochondria ROS Overproduction, and Inactivation of EGFR-Related Signalling Pathways.

Yu-Chi Chen, Po-Yu Wang, Bu-Miin Huang, Yu-Jen Chen, Wei-Chang Lee, Yung-Chia Chen

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. The PI3K Inhibitor HCD Promotes Caspase Activation in Head and Neck Squamous Cells by Upregulating the Extrinsic and Intrinsic Apoptosis Pathways.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026
    Article
  2. Review
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  7. Clerodane Diterpenoids from an Edible PlantMolecules (Basel, Switzerland) · 2021
    Article
  8. Phytochemicals fromMolecules (Basel, Switzerland) · 2021
    Review
  9. 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

6 authors at 3 institutions in 1 country.

Yu-Chi ChenDepartment of Urology, E-Da Cancer Hospital, Kaohsiung 824410, Taiwan.
Po-Yu WangDepartment of Paediatric Emergency, Changhua Christian Children Hospital, Changhua 500209, Taiwan.
Bu-Miin HuangDepartment of Anatomy, College of Medicine, National Cheng Kung University, Tainan 701401, Taiwan.
Yu-Jen ChenResen Biomedical Informatics Inc., Taipei 100043, Taiwan.
Wei-Chang LeeGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan.
Yung-Chia ChenGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan.ORCID 0000-0002-1953-4614
Kaohsiung Medical University · TWChanghua Christian Hospital · TWNational Cheng Kung University · TW

Funding

Changhua Christian Hospital 108-CCH-IRP-036E-Da Hosipital EDAHP108023Kaohsiung Medical University KMU107015, KMU108024Kaohsiung Medical University PT106001
6 · The paper itself

Abstract

A clerodane diterpene compound 16-hydroxycleroda-3,13-dien-15,16-olide (CD) is considered a therapeutic agent with pharmacological activities. The present study investigated the mechanisms of CD-induced apoptosis in T24 human bladder cancer cells. CD inhibited cell proliferation in a concentration and time-dependent manner. CD-induced overproduction of reactive oxygen species and reduced mitochondrial membrane potential, associated with reduced expression of Bcl-2 and increased levels of cytosolic cytochrome c, cleaved PARP-1 and caspase-3. In addition, CD treatment led to cell cycle arrest at the G0/G1 phase and inhibited expression of cyclin D1 and cyclin-dependent kinases 2 and 4 and led to increased levels of p21, p27Kip1 and p53. All of these events were accompanied with a reduction of pEGFR, pMEK1/2, pERK1/2, pAkt, pmTOR, pP70S6K1, HIF-1α, c-Myc and VEGF. RNAseq-based analysis revealed that CD-induced cell death was characterised by an increased expression of stress and apoptotic-related genes as well as inhibition of the cell cycle-related genes. In summary, CD induces apoptosis in T24 bladder cancer cells through targeting multiple intracellular signaling pathways as a result of oxidative stress and cell cycle arrest.

Indexed as

Antineoplastic AgentsApoptosisCell Cycle CheckpointsCell Line, TumorDiterpenes, ClerodaneErbB ReceptorsHumansMitochondriaPolyalthiaReactive Oxygen SpeciesSignal TransductionUrinary Bladder NeoplasmsAntineoplastic AgentsDiterpenes, ClerodaneEGFR protein, humanErbB ReceptorsReactive Oxygen Speciesapoptosisbladder cancercell cycleclerodane diterpeneepidermal growth factor receptor

Identifiers

PMID32872665
PMCPMC7504739
OpenAlexW3081694053

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.