Evidence map›Paper›PMID 41643630›Full record

ArticleTranslational oncology2026

Oncogenic role of talin-1 in glioma: Association with poor prognosis and regulation of the TGF-beta signaling pathway.

Jiayuan Li, Dongdong Zhang, Huandi Zhou, Liubing Hou, Yu Wang, Zizhou Zhang, Yanqiang Wang, Xiuwu Li, Le Yi, Xiaomin Liu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Jiayuan LiDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China.
Dongdong ZhangDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China; Brain Oncology Center, Hefei Cancer Hospital; Chinese Academy of Sciences, Hefei 230031, China.
Huandi ZhouDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China; Hebei Key Laboratory of Etiology Tracing and Individualized Diagnosis and Treatment for Digestive System Carcinoma, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 Hebei Province, China; Department of Central Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 Hebei, China.
Liubing HouDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China; Department of Central Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 Hebei, China.
Yu WangDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China.
Zizhou ZhangDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China.
Yanqiang WangDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China.
Xiuwu LiDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China.
Le YiDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 Hebei, China.
Xiaomin LiuHead and Neck Neuro-Oncology Center, Tianjin Huanhu Hospital, Tianjin, China.
Yongzhi WangBeijing Neurosurgical Institute, Beijing 100070, China.
Xiaoying XueDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang,050000 Hebei, China; Hebei Key Laboratory of Etiology Tracing and Individualized Diagnosis and Treatment for Digestive System Carcinoma, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000 Hebei Province, China. Electronic address: xxy0636@hebmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TLN1, a cytoskeletal protein associated with various tumors, remains inadequately studied in gliomas. In this study, we examined the functional role and mechanisms of TLN1 in glioma pathogenesis. Utilizing public databases, we conducted differential expression, survival (Kaplan-Meier/ROC), and regression analyses, which were subsequently validated with institutional datasets and clinical tissues. In vitro experiments demonstrated that TLN1 knockdown in glioma cells resulted in reduced proliferation (CCK8/EDU), migration and invasion (wound healing/Transwell), and increased apoptosis (AO/EB/flow cytometry); these findings were corroborated by Western blot analyses. Gene Set Enrichment Analysis (GSEA) linked TLN1 to the TGF-beta signaling pathway, a connection further validated by Western blot and in vivo murine models. Both public and institutional data indicated that TLN1 was upregulated in gliomas, with elevated expression correlating with poor prognosis. Furthermore, TLN1 knockdown inhibited glioma growth and progression in vitro and in vivo, primarily through the TGF-beta signaling pathway. Our findings establish TLN1 as an oncogenic driver in gliomas and highlight its potential as a therapeutic target.

Indexed as

GliomaProgressionTGF-beta signaling pathwayTLN1

Identifiers

PMID41643630
PMCPMC12903198

What Socratic holds

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LicenceCC BY-NC-ND
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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.