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Necrotic Cells Alter IRE1α-XBP1 Signaling and Induce Transcriptional Changes in Glioblastoma

Title
Necrotic Cells Alter IRE1α-XBP1 Signaling and Induce Transcriptional Changes in Glioblastoma
Authors
Lim J.; Lee S.; Hong Y.-S.; Choi J.H.; Jo A.; Kang J.L.; Song T.-J.; Choi Y.-H.
Ewha Authors
이지희; 최윤희; 최지하; 송태진; 임지우; 조아라
SCOPUS Author ID
이지희scopus; 최윤희scopus; 최지하scopus; 송태진scopus; 임지우scopus; 조아라scopus
Issue Date
2026
Journal Title
International Journal of Molecular Sciences
ISSN
1661-6596JCR Link
Citation
International Journal of Molecular Sciences vol. 27, no. 1
Keywords
endoplasmic reticulum stress; glioblastoma; IRE1α-XBP1 signaling; necrosis; unfolded protein response
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Necrosis is a characteristic feature of glioblastoma multiforme (GBM) and is closely associated with tumor-associated inflammation and poor clinical outcomes. However, the molecular consequences of necrotic cell death on endoplasmic reticulum (ER) stress signaling in GBM cells remain unclear. In this study, we examined the effects of necrotic cells on the ER stress signaling and unfolded protein response (UPR) in human glioblastoma cell lines. Exposure to necrotic cells reduced IRE1α phosphorylation and increased unspliced XBP1 (XBP1u) accumulation, without affecting PERK or ATF6 pathways. These changes were accompanied by enhanced IκBα phosphorylation and impaired autophagic degradation. Treatment with ER stress inducers failed to reverse XBP1u accumulation, and reduced phosphorylation of PKAc was observed together with decreased IRE1α activation. Transcriptomic analysis and quantitative reverse transcription PCR (qRT-PCR) revealed that necrotic cell-induced XBP1u was associated with altered expression of XBP1-related genes, while XBP1 knockdown produced similar transcriptional changes and enhanced the effects of necrotic cell treatment. These findings suggest that necrotic cells impair canonical IRE1α-XBP1 signaling and induce transcriptional reprogramming in glioblastoma cells, which may contribute to tumor progression. © 2026 by the authors.
DOI
10.3390/ijms27010474
Appears in Collections:
의과대학 > 의학과 > Journal papers
Files in This Item:
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