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pmid:40110305

The function of TRIML2 on the temozolomide resistance in glioblastoma.

Qiang Fu · Peipei Chen · Zening Wang · Bo Liu · Qingjiu Zhou · Ilhamjan Anwar · Yongxin Wang

Annals of medicine and surgery (2012) · 2025 doi:10.1097/MS9.0000000000002888

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Experiment

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Analysis

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title
The function of TRIML2 on the temozolomide resistance in glioblastoma.
doi
10.1097/MS9.0000000000002888
pmid
40110305
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Qiang Fu
[1]
Peipei Chen
[2]
Zening Wang
[3]
Bo Liu
[4]
Qingjiu Zhou
[5]
Ilhamjan Anwar
[6]
Yongxin Wang
journal
Annals of medicine and surgery (2012)
year
2025
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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l activity assays, wound-healing assays, and western blotting. The alteration of resistance to temozolomid
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mmunofluorescence, immunohistochemistry, and western blotting. Results: The expression of TRIML2 was signi
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ML2 in the resistant cell line by lentiviral transfection. The differences in TRIML2 expression betwee
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of our hospital. Cell culture and lentiviral transfection The human glioma cell line U87 was obtained
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therapy were verified by immunofluorescence, immunohistochemistry, and western blotting. Results: The expressi
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Complete file
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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.\nMethods: 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. 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