دورية أكاديمية
Temozolomide Resistance in Glioblastoma by NRF2: Protecting the Evil.
| العنوان: | Temozolomide Resistance in Glioblastoma by NRF2: Protecting the Evil. |
|---|---|
| المؤلفون: | Almeida Lima K; Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil., Osawa IYA; Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil., Ramalho MCC; Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil., de Souza I; Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil., Guedes CB; Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil., Souza Filho CHD; Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil., Monteiro LKS; Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil., Latancia MT; Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-3371, USA., Rocha CRR; Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil. |
| المصدر: | Biomedicines [Biomedicines] 2023 Apr 03; Vol. 11 (4). Date of Electronic Publication: 2023 Apr 03. |
| نوع المنشور: | Journal Article; Review |
| اللغة: | English |
| بيانات الدورية: | Publisher: MDPI AG Country of Publication: Switzerland NLM ID: 101691304 Publication Model: Electronic Cited Medium: Print ISSN: 2227-9059 (Print) Linking ISSN: 22279059 NLM ISO Abbreviation: Biomedicines Subsets: PubMed not MEDLINE |
| أسماء مطبوعة: | Original Publication: Basel, Switzerland : MDPI AG, [2013]- |
| مستخلص: | The transcription factor NRF2 is constitutively active in glioblastoma, a highly aggressive brain tumor subtype with poor prognosis. Temozolomide (TMZ) is the primary chemotherapeutic agent for this type of tumor treatment, but resistance to this drug is often observed. This review highlights the research that is demonstrating how NRF2 hyperactivation creates an environment that favors the survival of malignant cells and protects against oxidative stress and TMZ. Mechanistically, NRF2 increases drug detoxification, autophagy, DNA repair, and decreases drug accumulation and apoptotic signaling. Our review also presents potential strategies for targeting NRF2 as an adjuvant therapy to overcome TMZ chemoresistance in glioblastoma. Specific molecular pathways, including MAPKs, GSK3β, βTRCP, PI3K, AKT, and GBP, that modulate NRF2 expression leading to TMZ resistance are discussed, along with the importance of identifying NRF2 modulators to reverse TMZ resistance and develop new therapeutic targets. Despite the significant progress in understanding the role of NRF2 in GBM, there are still unanswered questions regarding its regulation and downstream effects. Future research should focus on elucidating the precise mechanisms by which NRF2 mediates resistance to TMZ, and identifying potential novel targets for therapeutic intervention. |
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| فهرسة مساهمة: | Keywords: NRF2; glioblastoma; temozolomide |
| تواريخ الأحداث: | Date Created: 20230516 Latest Revision: 20230519 |
| رمز التحديث: | 20240628 |
| مُعرف محوري في PubMed: | PMC10136186 |
| DOI: | 10.3390/biomedicines11041081 |
| PMID: | 37189700 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 2227-9059 |
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| DOI: | 10.3390/biomedicines11041081 |