Evidence map›Paper›PMID 40390043›Full record

ArticleChinese neurosurgical journal2025

The role of FAM111B in the malignant progression and molecular regulation of human glioma through the PI3K/Akt pathway.

Heng Wang, Junrou Zhu, Haiyang Wang, Wenhao Zheng, Linjie Wang, Jinhao Zhu, Zheng Wang, Quan Du

Abstract read
In one paragraph

Article in Chinese neurosurgical journal, 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

8 authors.

Heng WangThe Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
Junrou ZhuThe Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
Haiyang WangDepartment of Neurosurgery, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, China.
Wenhao ZhengDepartment of Neurosurgery, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, China.
Linjie WangThe Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
Jinhao ZhuThe Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
Zheng WangThe Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
Quan DuDepartment of Neurosurgery, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, China. duquan76@163.com.

Funding

agricultural and social development project of Hangzhou no. 20211231Y025agricultural and social development project of Hangzhou no. 202204B11Zhejiang Traditional Chinese Medicine Administration no. 851100G02309;no. 851100G02312
6 · The paper itself

Abstract

backgroundGliomas represent the most prevalent primary neoplasm in the adult central nervous system. Despite advancements in therapeutic modalities, such as surgical intervention, radiotherapy, chemotherapy, and tumor treatment, the 5-year survival rate of glioma patients remains low. Therefore, there is an urgent need to develop additional treatment methods. Recent studies have suggested that FAM111B is involved in DNA repair, cell cycle regulation, and apoptosis. FAM111B mutations and overexpression are related to cancer.

methodsWe found that FAM111B was significantly overexpressed in glioma tissues compared to the adjacent tissues by analyzing data from the TCGA_GBM&LGG and CGGA databases. Moreover, overexpression of FAM111B was associated with shorter overall survival, and disease-specific survival and tended to increase with disease stage progression. Cellular experiments confirmed these results. These results suggest that overexpression of FAM111B promotes the proliferation, migration, and invasion of glioma cells, whereas the knockdown of FAM111B inhibits these activities. We also found that FAM111B regulated glioma cell proliferation, migration, and invasion via the PI3K/AKT pathway.

resultsFAM111B is capable of enhancing the proliferation, invasion, and migration capabilities of glioma cells and promotes the malignant progression of glioma via the PI3K/Akt signaling pathway.

conclusionsThis is the first study to demonstrate that FAM111B plays a crucial role in the proliferation, migration, and invasion of glioma cells. The malignant phenotype of FAM111B has also been shown to be closely associated with the PI3K/AKT pathway. FAM111B may be a predictive biomarker and a potential therapeutic target for gliomas.

Identifiers

PMID40390043
PMCPMC12087166

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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.