Evidence map›Paper›PMID 39819316›Full record

ArticleMolecular medicine (Cambridge, Mass.)2025

Nootkatone inhibits the progression of glioblastoma by activating the ATF4-CHOP-CHAC1 pathway.

Qian Wang, Xiumin Xue, Zhichao Chen, Wei Zhang, Yiming Qian, Danni Chen, Lin Lin, Yinfeng Yuan, Weiqiao Zhao, Zhihui Huang and 1 more

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

11 authors.

Qian Wang *School of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Xiumin Xue *School of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Zhichao ChenSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Wei ZhangSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Yiming QianSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Danni ChenSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Lin LinSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Yinfeng YuanSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Weiqiao ZhaoSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China.
Zhihui HuangSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China. huang0069@hznu.edu.cn.
Yongjie WangSchool of Pharmacy, Hangzhou Normal University, Hangzhou, 311121, China. wangyongjie@hznu.edu.cn.

Funding

Medical Science and Technology Project of Zhejiang Province 2023RC074Medical Science and Technology Project of Zhejiang Province 2024KY244Ministry of Science and Technology China Brain Initiative Grant 2022ZD0204700the National Natural Science Foundation of China 82071230the Natural Science Foundation of Zhejiang Province LY23H090001
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) represents a primary brain tumor that is widely prevalent, and clinical drugs available for its treatment exhibit varying degrees of resistance. Nootkatone (NKT) is a functional sesquiterpene sourced from traditional Chinese medicine --Alpinia Oxyphylla Miq and has been reported to have a diverse range of pharmacological properties. However, it remains unknown whether there are effects of NKT on GBM. In this study, we found that NKT inhibited the growth of GBM cells in a dose-dependent manner in vitro. Subsequently, we observed that NKT suppressed the migration and arrested cell cycle at G2/M phase of GBM cells. Furthermore, NKT induced the death of GBM cells accompanied by an increase in reactive oxygen species (ROS) production. Mechanistically, we found that NKT inhibited the progression of GBM cells through activating the ATF4-CHOP-CHAC1 pathway in GBM cells. Furthermore, NKT-induced inhibition of migration and proliferation in GBM cells was partially restored by ATF4 or CHAC1 knockdown. Finally, we found that NKT inhibited the growth of tumor in GBM orthotopic mice model through activation of ATF4-CHOP-CHAC1 axis. Taken together, our findings show that NKT suppresses the growth and migration of GBM cells by activating the ATF4-CHOP-CHAC1 pathway, which in turn prevents the tumorigenesis of GBMs and provides a novel perspective for the development of drugs against GBM.

Indexed as

Activating Transcription Factor 4Brain NeoplasmsGlioblastomaPolycyclic SesquiterpenesSesquiterpenesSignal TransductionTranscription Factor CHOPAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionHumansMiceMice, NudeReactive Oxygen SpeciesActivating Transcription Factor 4ATF4 protein, humanDDIT3 protein, humanPolycyclic SesquiterpenesReactive Oxygen SpeciesSesquiterpenesTranscription Factor CHOPATF4-CHOP-CHAC1Glioblastoma multiformeNootkatoneProliferationROS

Identifiers

PMID39819316
PMCPMC11737244

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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.