ArticleAnnals of medicine and surgery (2012)2025
The function of TRIML2 on the temozolomide resistance in glioblastoma.
Article in Annals of medicine and surgery (2012), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Structure-Guided Design of Cyclic Peptide: A Potent Inhibitor Targeting PD-1/PD-L1 Axis with Antitumor Activity.International journal of molecular sciences · 2025Article
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7 authors.
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Abstract
Background: Acquired resistance to temozolomide is a major challenge for the effective treatment of glioblastoma (GBM). TRIML2, a member of the TRIM family, plays an important role in cancer genesis, progression, and treatment resistance. However, its mechanism of action in GBM resistance to temozolomide remains unclear. Methods: RNA bulk sequencing data from temozolomide-resistant U87 cells and wild-type U87 cells were downloaded from the NCBI public database (GEO: GSE193957) and analyzed. A temozolomide-resistant cell line (U87-TR) was induced with temozolomide, and the expression of TRIML2 in temozolomide-resistant and wild-type cell lines (U87-WT) was verified by cell activity assays, wound-healing assays, and western blotting. The alteration of resistance to temozolomide was assessed following the overexpression of TRIML2 in the resistant cell line by lentiviral transfection. The differences in TRIML2 expression between primary GBM and recurrent GBM after temozolomide chemotherapy were verified by immunofluorescence, immunohistochemistry, and western blotting. Results: The expression of TRIML2 was significantly lower in U87-TR cells than in U87-WT cells. After the TRIML2 overexpressed in U87-TR cells, their resistance to temozolomide was significantly decreased and became sensitive to temozolomide treatment. TRIML2 expression was significantly decreased in the temozolimide-resistant GBM tumors; in contrast, TRIML2 was relatively high expressed in the temozolimide-sensitive GBM tumors. Conclusions: TRIML2 inhibits temozolomide resistance in GBM and thus may serve as a novel therapeutic target for overcoming GBM resistance to temozolomide.
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