Hierarchical Disruption of the Tryptophan-Melatonin Axis Contributes to Glioma Progression Through AKT/ERK/STAT3 Signalling.
Overview
- Department of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China
- Department of Endocrinology, Guangyuan Central Hospital, Guangyuan, Sichuan, China
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/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper says that its authors' code is available on request: it was not published with the paper, so there is nothing to verify.
The paper's code and data availability statement is in the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none (its code is available on request), so it has no map.
Data
No dataset and no data link were found in the paper.
Data Availability Statement
The data that support the findings of this study are available from the corresponding author upon reasonable request.
Reproduced under the paper's license (CC BY), from the paper cited above.
Ethical Considerations and Data Availability
All bioinformatic analyses were conducted using publicly available, de‐identified datasets. Experimental validation was performed using archived anonymized human glioma tissue specimens and established glioma cell lines. No prospective human recruitment or animal experiments were involved in this study. The use of archived human specimens was approved by the institutional ethics committee, and the requirement for informed consent was waived in accordance with institutional policies and national regulations. Processed data and analysis scripts are available from the corresponding author upon reasonable request.
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 12 authors, 9 keywords, 15 MeSH terms, 4 funders, 36 references.
Cite
This paper
Tan, B., Yao, S., He, S., Chen, T., Chen, H., Yang, W., Tang, X., Xu, T., Zhang, J., Yin, X., Chen, Y., & Song, P. (2026). Hierarchical Disruption of the Tryptophan-Melatonin Axis Contributes to Glioma Progression Through AKT/
BibTeX
@article{tan2026hierarch
author = {Tan, Bo and Yao, Suqiu and He, Shuangyin and Chen, Tao and Chen, Han and Yang, Wenfu and Tang, Xiyuan and Xu, Tingting and Zhang, Jiajie and Yin, Xiaohong and Chen, Ying and Song, Peng},
title = {{Hierarchical Disruption of the Tryptophan-Melatonin Axis Contributes to Glioma Progression Through AKT/
journal = {Journal of cellular and molecular medicine},
year = {2026},
month = jun,
volume = {30},
number = {11},
pages = {e71243},
publisher = {Wiley},
issn = {1582-1838},
doi = {10.1111/
url = {https://
pmid = {42286740},
pmcid = {PMC13263238}
}
RIS
TY - JOUR
AU - Tan, Bo
AU - Yao, Suqiu
AU - He, Shuangyin
AU - Chen, Tao
AU - Chen, Han
AU - Yang, Wenfu
AU - Tang, Xiyuan
AU - Xu, Tingting
AU - Zhang, Jiajie
AU - Yin, Xiaohong
AU - Chen, Ying
AU - Song, Peng
TI - Hierarchical Disruption of the Tryptophan-Melatonin Axis Contributes to Glioma Progression Through AKT/
T2 - Journal of cellular and molecular medicine
J2 - J Cell Mol Med
PY - 2026
DA - 2026/
VL - 30
IS - 11
SP - e71243
SN - 1582-1838
PB - Wiley
DO - 10.1111/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1111/
"type": "article-journal",
"title": "Hierarchical Disruption of the Tryptophan-Melatonin Axis Contributes to Glioma Progression Through AKT/
"container-title": "Journal of cellular and molecular medicine",
"author": [
{
"family": "Tan",
"given": "Bo"
},
{
"family": "Yao",
"given": "Suqiu"
},
{
"family": "He",
"given": "Shuangyin"
},
{
"family": "Chen",
"given": "Tao"
},
{
"family": "Chen",
"given": "Han"
},
{
"family": "Yang",
"given": "Wenfu"
},
{
"family": "Tang",
"given": "Xiyuan"
},
{
"family": "Xu",
"given": "Tingting"
},
{
"family": "Zhang",
"given": "Jiajie"
},
{
"family": "Yin",
"given": "Xiaohong"
},
{
"family": "Chen",
"given": "Ying"
},
{
"family": "Song",
"given": "Peng"
}
],
"container-title-short":
"volume": "30",
"issue": "11",
"page": "e71243",
"DOI": "10.1111/
"PMID": "42286740",
"PMCID": "PMC13263238",
"ISSN": "1582-1838",
"publisher": "Wiley",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
6,
1
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1038/s41586-026-10631-3 [code]
- A prognostic human brain network for diffuse midline glioma.Journal: NatureIn common: other condition, 1 reference
- [2] doi:10.1038/s43587-026-01207-x [code]
- A microprotein atlas of the human frontal cortex in Alzheimer's disease.Journal: Nature agingIn common: 1 reference
- [3] doi:10.1038/s41597-026-07270-8 [code]
- Whole-genome DNA methylation profile of female Gobiocypris rarus brains at three age stages.Journal: Scientific dataIn common: 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.
