Evidence map›Paper›PMID 36572650›Full record

ReviewPharmacology research & perspectives2023

Xanthatin suppresses proliferation and tumorigenicity of glioma cells through autophagy inhibition via activation of the PI3K-Akt-mTOR pathway.

Huaqing Chen, Tong Zhu, Xiaojie Huang, Wenshuang Xu, Zemin Di, Yuyang Ma, Min Xue, Sixing Bi, Yujun Shen, Yongqiang Yu and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in Pharmacology research & perspectives, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Huaqing ChenSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Tong ZhuSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Xiaojie HuangSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Wenshuang XuSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Zemin DiSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Yuyang MaSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Min XueSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Sixing BiInstitute of Biopharmaceuticals, Anhui Medical University, Hefei, China.
Yujun ShenSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Yongqiang YuThe First Affiliated Hospital of Anhui Medical University, Hefei, China.
Yuxian ShenSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Lijie FengSchool of Basic Medical Sciences, Anhui Medical University, Hefei, China.ORCID 0000-0002-0845-2541
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is the most common and aggressive primary brain tumor in adults with high morbidity and mortality. Rapid proliferation and diffuse migration are the main obstacles to successful glioma treatment. Xanthatin, a sesquiterpene lactone purified from Xanthium strumarium L., possesses a significant antitumor role in several malignant tumors. In this study, we report that xanthatin suppressed glioma cells proliferation and induced apoptosis in a time- and concentration-dependent manner, and was accompanied by autophagy inhibition displaying a significantly reduced LC3 punctate fluorescence and LC3II/I ratio, decreased level of Beclin 1, while increased accumulation of p62. Notably, treating glioma cells with xanthatin resulted in obvious activation of the PI3K-Akt-mTOR signaling pathway, as indicated by increased mTOR and Akt phosphorylation, decreased ULK1 phosphorylation, which is important in modulating autophagy. Furthermore, xanthatin-mediated pro-apoptosis in glioma cells was significantly reversed by autophagy inducers (rapamycin or Torin1), or PI3K-mTOR inhibitor NVP-BEZ235. Taken together, these findings indicate that anti-proliferation and pro-apoptosis effects of xanthatin in glioma are most likely by inhibiting autophagy via activation of PI3K-Akt-mTOR pathway, suggesting a potential therapeutic strategy against glioma.

Indexed as

GliomaProto-Oncogene Proteins c-aktAutophagyCell Line, TumorFuransHumansPhosphatidylinositol 3-KinasesTOR Serine-Threonine KinasesFuransMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesxanthatinautophagygliomamTORtumorigenicityxanthatin

Identifiers

PMID36572650
PMCPMC9792428
OpenAlexW4312197962

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.