Evidence map›Paper›PMID 40295200›Full record

ArticleJournal of microbiology and biotechnology2025

Cynaropicrin Suppresses Cell Proliferation by Inducing Mitophagy through p38 MAPK-Mediated Mitochondrial ROS Generation in Human Hepatocellular Carcinoma Cells.

Min Yeong Kim, Hyun Hwangbo, Seon Yeong Ji, Da Hye Kim, Shin-Hyung Park, Su Hyun Hong, Gi Young Kim, EunJin Bang, Yung Hyun Choi

Abstract read
In one paragraph

Article in Journal of microbiology and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Min Yeong KimBasic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Hyun HwangboBasic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Seon Yeong JiBasic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Da Hye KimBasic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Shin-Hyung ParkDepartment of Pathology, Dong-eui University College of Korean Medicine, Busan 47227, Republic of Korea.
Su Hyun HongBasic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Gi Young KimLaboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Jeju 63243, Republic of Korea.
EunJin BangBasic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Yung Hyun ChoiBasic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cynaropicrin, a sesquiterpene lactone, has diverse pharmacological activities. However, its anticancer activity against hepatocellular carcinoma (HCC) has not been fully elucidated. Here, we investigated the cytotoxic effects of cynaropicrin and examined its mechanism of action in human HCC cells. The results demonstrated that cynaropicrin significantly induced cytotoxicity and autophagy in HCC cells, but not in immortalized non-cancerous hepatocytes, which was related to the generation of mitochondrial reactive oxygen species (mtROS) and induction of mitochondrial membrane potential loss. Under cynaropicrin treatment, the expression of microtubule-associated protein light chain 3, which is involved in the elongation of the phagophore membrane, was upregulated, whereas the expression of Beclin-1 and p62, which are essential for the formation of autophagosomes, was downregulated. In addition, the expression of mitophagy regulators PTEN-induced kinase 1 (PINK1) and Parkin in the mitochondria increased, suggesting the induction of autophagic flux in the mitochondria. However,

Indexed as

Carcinoma, HepatocellularCell ProliferationLactonesLiver NeoplasmsMitochondriaMitophagyp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesSesquiterpenesAutophagyCell Line, TumorHumansMembrane Potential, MitochondrialProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein LigasesLactonesp38 Mitogen-Activated Protein Kinasesparkin proteinProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesSesquiterpenesUbiquitin-Protein LigasesCynaropicrinhepatocellular carcinoma cellsmitophagyp38 MAPKreactive oxygen species

Identifiers

PMID40295200
PMCPMC12089954

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Registered trials

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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.