Evidence map›Paper›PMID 41316197›Full record

ArticleCancer cell international2025

Elevated expression and secretion of TGF-α contribute to Temozolomide resistance in human glioblastoma cells.

Jen-Tsung Yang, I-Neng Lee, Ming-Shan Chen, Cheng Huang, Hsiu-Chen Huang, Yu-Ping Wu, Jui-Chieh Chen

Abstract read
In one paragraph

Article in Cancer cell international, 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

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

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

7 authors.

Jen-Tsung YangDepartment of Neurosurgery, Chang Gung Memorial Hospital, Chiayi, 61363, Taiwan.
I-Neng LeeDepartment of Medical Research, Chang Gung Memorial Hospital, Chiayi, 61363, Taiwan.
Ming-Shan ChenDepartment of Anesthesiology, Ditmanson Medical Foundation Chia‑Yi Christian Hospital, Chiayi, 60002, Taiwan.
Cheng HuangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang Ming Chiao Tung University, Taipei, 11221, Taiwan.
Hsiu-Chen HuangDepartment of Applied Science, National Tsing Hua University South Campus, Hsinchu, Taiwan.
Yu-Ping WuDepartment of Medical Research, Chang Gung Memorial Hospital, Chiayi, 61363, Taiwan.
Jui-Chieh ChenDepartment of Biochemical Science and Technology, National Chiayi University, Chiayi, 600355, Taiwan. jcc@mail.ncyu.edu.tw.

Funding

Chang Gung Medical Research Council CMRPG6K0063
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is a highly aggressive brain tumor often treated with Temozolomide (TMZ). Research reveals that secretory substances and receptor-activated signaling may contribute to TMZ resistance in GBM cells. RNA-Seq and bioinformatics analyses reveal that TMZ treatment downregulates most genes, particularly those involved in cell structure and metabolism, while activating genes linked to secretory substances like cytokines, chemokines, and growth factors. Antibody array analysis identified a significant increase in TGF-α secretion after TMZ treatment, which also triggered its associated pathways. Moreover, the remarkable secretion of TGF-α also triggered the activation of its associated pathways. Notably, a marked increase in TGF-α expression was observed in TMZ-resistant cells. TGF-α knockdown restored TMZ sensitivity in a mouse xenograft model. Tissue analysis revealed significantly higher TGF-α levels in GBM, suggesting its potential as a drug resistance biomarker and target for new therapies.

Indexed as

Drug resistanceGlioblastoma (GBM)Protein secretionTemozolomide (TMZ)Transforming growth factor-alpha (TGF-α)

Identifiers

PMID41316197
PMCPMC12661727

What OpenQuestion 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 OpenQuestion graph.