ArticleMedComm2026
Inhibition of FOS-Like Antigen 1 Reduces Chemoresistance to Temozolomide Through Stemness Reprogramming via IL-6/STAT3
Article in MedComm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
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Who cites it
2 citing papers in PubMed.
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most lethal brain tumor, characterized by strong resistance to conventional therapies. Despite recent therapeutic advancements, overcoming chemoresistance remains a major challenge. Here, we identified FOS-like antigen 1 (FOSL1) as a novel therapeutic target in GBM, particularly in patients with resistance to conventional drugs, including temozolomide (TMZ). FOSL1 gene was identified from the DepMap database as a potential mediator of TMZ resistance in GBM and found to be associated with chemoresistance molecular signatures and poor clinical outcomes. Functional analyses in GBM cells revealed that FOSL1 suppression enhanced apoptosis, induced G0/G1 cell cycle arrest, and reduced both cell migration and stemness marker expression. Transcriptomic profiling, including single-cell RNA-seq and bulk RNA-seq, highlighted the pivotal role of the interleukin-6 (IL-6)/STAT3 signaling pathway in FOSL1-mediated stemness. Mechanistically, in vitro experiments demonstrated that FOSL1 induces GBM stemness through IL-6-pSTAT3
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