Evidence map›Paper›PMID 41326907›Full record

ArticleCNS neuroscience & therapeutics2025

Traditional Chinese Medicinal Leech Induces Apoptosis and Autophagy in Glioblastoma by SGK1/Caspase-3 and PI3K/AKT/mTOR Pathway.

Shaohua Wu, Yaya Zhou, Zhuan Pei, Yang Wang, Zuping Zhang

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 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

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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. 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

5 authors.

Shaohua WuDepartment of Parasitology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, People's Republic of China.
Yaya ZhouDepartment of Parasitology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, People's Republic of China.
Zhuan PeiDepartment of Neurology, the Third Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Yang WangInstitute of Integrative Medicine, Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.ORCID 0000-0003-0447-3107
Zuping ZhangDepartment of Parasitology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, People's Republic of China.

Funding

Scientific Research Program of Hunan Provincial Health Commission A202301066295
6 · The paper itself

Abstract

backgroundGlioblastoma (GBM) represents the most lethal form of high-grade glioma, with current therapeutic options proving largely ineffective. Consequently, there is an urgent need for novel treatment strategies. Recent studies have indicated that the medicinal leech exhibits notable anticancer properties. However, the precise mechanisms underlying these effects remain to be elucidated.

methodsTo investigate the impact of leech drug-containing serum (LDS) on the proliferation, migration, and invasion of GBM cells, a series of assays including CCK-8, ethynyl deoxyuridine (EdU), colony formation, scratch, and transwell assays were employed. Additionally, the apoptosis and autophagy of GBM cells were analyzed using flow cytometry, monodansylcadaverine staining and the immunofluorescence assay. Transcriptomic sequencing of the cells was conducted to identify differentially expressed genes. In vivo, anticancer activity was assessed by developing tumor xenograft models. Western blot analysis was utilized to identify proteins associated with apoptosis and autophagy.

resultsLeech drug-containing serum (LDS) significantly inhibited proliferation, migration, and invasion. Furthermore, it induced autophagy and apoptosis in GBM. Differential gene enrichment analysis and pathway validation indicated that LDS exerts anti-GBM effects by modulating the PI3K/AKT pathway. Leech extracts effectively inhibit the growth of GBM in a subcutaneous xenograft tumor model.

conclusionThe leech-derived compounds may induce apoptosis and autophagy in GBM by modulating the PI3K/AKT/mTOR signaling pathway, without eliciting significant adverse effects, thereby presenting itself as a promising therapeutic agent.

Indexed as

ApoptosisAutophagyBrain NeoplasmsGlioblastomaLeechesAnimalsCaspase 3Cell Line, TumorCell MovementCell ProliferationHumansMiceMice, Inbred BALB CMice, NudePhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesCaspase 3MTOR protein, humanPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesapoptosisautophagyglioblastomaleech

Identifiers

PMID41326907
PMCPMC12668900

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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.