Evidence map›Paper›PMID 38739004›Full record

ArticleCNS neuroscience & therapeutics2024

TNF-α can promote membrane invasion by activating the MAPK/MMP9 signaling pathway through autocrine in bone-invasive pituitary adenoma.

Xinzhi Wu, Lei Gong, Bin Li, Jiwei Bai, Chuzhong Li, Yazhuo Zhang, Haibo Zhu

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
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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

7 authors.

Xinzhi WuBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Lei GongBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Bin LiDepartment of Neurosurgery, Peking University People's Hospital, Beijing, China.
Jiwei BaiDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Chuzhong LiBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Yazhuo ZhangBeijing Neurosurgical Institute, Capital Medical University, Beijing, China.ORCID 0000-0002-8583-2580
Haibo ZhuDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.ORCID 0000-0003-2191-375X

Funding

National Natural Science Foundation of China 82103028
6 · The paper itself

Abstract

aimsA bone-invasive pituitary adenoma exhibits aggressive behavior, leading to a worse prognosis. We have found that TNF-α promotes bone invasion by facilitating the differentiation of osteoclasts, however, before bone-invasive pituitary adenoma invades bone tissue, it needs to penetrate the dura mater, and this mechanism is not yet clear.

methodsWe performed transcriptome microarrays on specimens of bone-invasive pituitary adenomas (BIPAs) and noninvasive pituitary adenomas (NIPAs) and conducted differential expressed gene analysis and enrichment analysis. We altered the expression of TNF-α through plasmids, then validated the effects of TNF-α on GH3 cells and verified the efficacy of the TNF-α inhibitor SPD304. Finally, the effects of TNF-α were validated in in vivo experiments.

resultsPathway act work showed that the MAPK pathway was significantly implicated in the pathway network. The expression of TNF-α, MMP9, and p-p38 is higher in BIPAs than in NIPAs. Overexpression of TNF-α elevated the expression of MAPK pathway proteins and MMP9 in GH3 cells, as well as promoted proliferation, migration, and invasion of GH3 cells. Flow cytometry indicated that TNF-α overexpression increased the G2 phase ratio in GH3 cells and inhibited apoptosis. The expression of MMP9 was reduced after blocking the P38 MAPK pathway; overexpression of MMP9 promoted invasion of GH3 cells. In vivo experiments confirm that the TNF-α overexpression group has larger tumor volumes. SPD304 was able to suppress the effects caused by TNF-α overexpression.

conclusionBone-invasive pituitary adenoma secretes higher levels of TNF-α, which then acts on itself in an autocrine manner, activating the MAPK pathway and promoting the expression of MMP9, thereby accelerating the membrane invasion process. SPD304 significantly inhibits the effect of TNF-α and may be applied in the clinical treatment of bone-invasive pituitary adenoma.

Indexed as

AdenomaMAP Kinase Signaling SystemMatrix Metalloproteinase 9Neoplasm InvasivenessPituitary NeoplasmsTumor Necrosis Factor-alphaAdultAnimalsAutocrine CommunicationBone NeoplasmsCell Line, TumorCell MovementFemaleHumansMaleMiceMatrix Metalloproteinase 9MMP9 protein, humanTumor Necrosis Factor-alphabone invasionmembrane invasionpituitary adenomaSPD304TNF‐α

Identifiers

PMID38739004
PMCPMC11090077

What Socratic holds

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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 Socratic graph.