Evidence map›Paper›PMID 33350608›Full record

ArticleFEBS open bio2021

Osthole induces necroptosis via ROS overproduction in glioma cells.

Mengjie Huangfu, Riming Wei, Juan Wang, Jianli Qin, Dan Yu, Xiao Guan, Xumei Li, Minglei Fu, Haiping Liu, Xu Chen

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. The Small Molecules of Plant Origin with Anti-Glioma Activity.International journal of molecular sciences · 2025
    Review
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  5. Article
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  10. Animals : an open access journal from MDPI · 2022
    Article
  11. Review
  12. Article
  13. Emerging roles of ferroptosis in glioma.Frontiers in oncology · 2022
    Review
  14. Review
  15. 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

10 authors at 2 institutions in 1 country.

Mengjie HuangfuCollege of Pharmacy, Guilin Medical University, China.
Riming WeiInstitute of Biotechnology, Guilin Medical University, China.
Juan WangCollege of Pharmacy, Guilin Medical University, China.
Jianli QinCollege of Pharmacy, Guilin Medical University, China.
Dan YuCollege of Pharmacy, Guilin Medical University, China.
Xiao GuanCollege of Pharmacy, Guilin Medical University, China.
Xumei LiCollege of Pharmacy, Guilin Medical University, China.
Minglei FuThe Second Affiliated Hospital of Guilin Medical University, China.
Haiping LiuScience and Technology Department, Guilin Medical University, China.
Xu ChenCollege of Pharmacy, Guilin Medical University, China.ORCID 0000-0003-4910-9608
Guilin Medical University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is a common primary malignant tumor that has a poor prognosis and often develops drug resistance. The coumarin derivative osthole has previously been reported to induce cancer cell apoptosis. Recently, we found that it could also trigger glioma cell necroptosis, a type of cell death that is usually accompanied with reactive oxygen species (ROS) production. However, the relationship between ROS production and necroptosis induced by osthole has not been fully elucidated. In this study, we found that osthole could induce necroptosis of glioma cell lines U87 and C6; such cell death was distinct from apoptosis induced by MG-132. Expression of necroptosis inhibitor caspase-8 was decreased, and levels of necroptosis proteins receptor-interacting protein 1 (RIP1), RIP3 and mixed lineage kinase domain-like protein were increased in U87 and C6 cells after treatment with osthole, whereas levels of apoptosis-related proteins caspase-3, caspase-7, and caspase-9 were not increased. Lactate dehydrogenase release and flow cytometry assays confirmed that cell death induced by osthole was primarily necrosis. In addition, necroptosis induced by osthole was accompanied by excessive production of ROS, as observed for other necroptosis-inducing reagents. Pretreatment with the RIP1 inhibitor necrostatin-1 attenuated both osthole-induced necroptosis and the production of ROS in U87 cells. Furthermore, the ROS inhibitor N-acetylcysteine decreased osthole-induced necroptosis and growth inhibition. Overall, these findings suggest that osthole induces necroptosis of glioma cells via ROS production and thus may have potential for development into a therapeutic drug for glioma therapy.

Indexed as

ApoptosisBrain NeoplasmsCell Line, TumorCoumarinsDrug Screening Assays, AntitumorGliomaHumansLeupeptinsMembrane Potential, MitochondrialMitochondriaNecroptosisReactive Oxygen Speciesbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCoumarinsLeupeptinsostholReactive Oxygen Speciescell necroptosisgliomaostholeROS production

Identifiers

PMID33350608
PMCPMC7876487
OpenAlexW3114988789

What OpenQuestion holds

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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.