Evidence map›Paper›PMID 42286740›Full record

ArticleJournal of cellular and molecular medicine2026

Hierarchical Disruption of the Tryptophan-Melatonin Axis Contributes to Glioma Progression Through AKT/ERK/STAT3 Signalling.

Bo Tan, Suqiu Yao, Shuangyin He, Tao Chen, Han Chen, Wenfu Yang, Xiyuan Tang, Tingting Xu, Jiajie Zhang, Xiaohong Yin and 2 more

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Bo TanDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.ORCID 0000-0001-5976-7546
Suqiu YaoDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Shuangyin HeDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Tao ChenDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Han ChenDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Wenfu YangDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Xiyuan TangDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Tingting XuDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Jiajie ZhangDepartment of Endocrinology, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Xiaohong YinDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Ying ChenDepartment of Endocrinology, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Peng SongDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.

Funding

Guangyuan Science and Technology Bureau - Science and Technology Project 23ZDYF0053Health Commission of Sichuan Province Medical Science and Technology Program 24WSXT042Sichuan Provincial Clinical Key Specialty Construction Project 2024HSWKP001Wu Jieping Medical Foundation 320.6750.2024-6-113
6 · The paper itself

Abstract

Melatonin signalling, mediated by membrane receptors and tightly regulated biosynthetic enzymes, is a key component of circadian and neuroendocrine control in the brain. However, whether the tryptophan-melatonin axis remains hierarchically intact during glioma progression and how its disruption affects downstream signalling remain unclear. In this study, transcriptomic data from TCGA, CGGA, and GTEx were integrated to characterize the expression patterns of melatonin receptors (MTNR1A and MTNR1B) and biosynthetic enzymes (AANAT and ASMT) across normal brain tissue, lower-grade glioma and glioblastoma. Protein expression was validated by immunohistochemistry, and functional consequences were investigated through gain- and loss-of-function experiments in glioma cells, followed by proliferation, migration, invasion, apoptosis and signalling analyses. Multi-layered analyses revealed a coordinated disruption of the tryptophan-melatonin axis during glioma progression. Expression of AANAT, ASMT, MTNR1A and MTNR1B progressively declined with increasing tumour grade and was associated with poor prognosis. Immunohistochemistry confirmed reduced MTNR1A and ASMT protein expression in glioma tissues. Restoration of these factors suppressed glioma cell proliferation, migration and invasion while promoting apoptosis. Mechanistically, these effects were accompanied by inhibition of AKT, ERK and STAT3 signalling. These findings demonstrate that hierarchical disruption of receptor- and synthesis-dependent melatonin signalling is a defining molecular feature of glioma and may contribute to malignant progression through activation of AKT/ERK/STAT3 pathways, providing new insights into the biological and therapeutic relevance of the tryptophan-melatonin axis in glioma.

Indexed as

Brain NeoplasmsGliomaMelatoninProto-Oncogene Proteins c-aktSTAT3 Transcription FactorTryptophanApoptosisCell Line, TumorCell MovementCell ProliferationDisease ProgressionExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHumansSignal TransductionExtracellular Signal-Regulated MAP KinasesMelatoninProto-Oncogene Proteins c-aktSTAT3 protein, humanSTAT3 Transcription FactorTryptophanAKT signallingASMTERK pathwaygliomamelatoninmolecular mechanismMTNR1ASTAT3tumour progression

Identifiers

PMID42286740
PMCPMC13263238

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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.