ArticleCNS neuroscience & therapeutics2021
Regulation of temozolomide resistance in glioma cells via the RIP2/NF-κB/MGMT pathway.
Article in CNS neuroscience & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Ripk2 promotes CD8Cell death & disease · 2026Article
- Tβ4-17 peptide enhances the chemo-sensitivity of ovarian cancer cells to DDP by affecting NF-κB signaling pathway.Medical oncology (Northwood, London, England) · 2025Article
- Overcoming temozolomide resistance in glioma: recent advances and mechanistic insights.Acta neuropathologica communications · 2025Review
- LAMB1 downregulation suppresses glioma progression by inhibiting aerobic glycolysis through regulation of the NF-κB/HK2 axis.Discover oncology · 2025Article
- Temozolomide-Promoted MGMT Transcription Contributes to Chemoresistance by Activating the ERK Signalling Pathway in Malignant Melanoma.Journal of cellular and molecular medicine · 2025Article
- XPO1-inhibitor Selinexor induces MGMT expression by activating PKA-CREB signaling inFrontiers in oncology · 2025Article
- Current progress of anti‑PD‑1/PDL1 immunotherapy for glioblastoma (Review).Molecular medicine reports · 2024Review
- CD2AP promotes the progression of glioblastoma multiforme via TRIM5-mediated NF-kB signaling.Cell death & disease · 2024Article
- Molecular Determinants for Photodynamic Therapy Resistance and Improved Photosensitizer Delivery in Glioma.International journal of molecular sciences · 2024Review
- Transcriptomic analysis identifies the neuropeptide cortistatin (CORT) as an inhibitor of temozolomide (TMZ) resistance by suppressing the NF-κB-MGMT signaling axis in human glioma.Genes & diseases · 2024Article
- Genome-wide DNA methylation analysis identifies potent CpG signature for temzolomide response in non-G-CIMP glioblastomas with unmethylated MGMT promoter: MGMT-dependent roles of GPR81.CNS neuroscience & therapeutics · 2024Article
- Article
- Aloe-Emodin Overcomes Anti-Cancer Drug Resistance to Temozolomide and Prevents Colony Formation and Migration in Primary Human Glioblastoma Cell Lines NULU and ZAR.Molecules (Basel, Switzerland) · 2023Article
- The Recent Research Progress of NF-κB Signaling on the Proliferation, Migration, Invasion, Immune Escape and Drug Resistance of Glioblastoma.International journal of molecular sciences · 2023Review
- Article
- Iron Oxide Nanoparticles Decorated with Functional Peptides for a Targeted siRNA Delivery to Glioma Cells.ACS applied materials & interfaces · 2023Review
- RIPK2: a promising target for cancer treatment.Frontiers in pharmacology · 2023Review
- Mechanism of RIP2 enhancing stemness of glioma cells induces temozolomide resistance.CNS neuroscience & therapeutics · 2022Article
- The Novel Protein ADAMTS16 Promotes Gastric Carcinogenesis by Targeting IFI27 through the NF-κb Signaling Pathway.International journal of molecular sciences · 2022Article
- ADAR3 activates NF-κB signaling and promotes glioblastoma cell resistance to temozolomide.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTemozolomide (TMZ) is a first-line chemotherapy drug for the treatment of malignant glioma and resistance to it poses a major challenge. Receptor-interacting protein 2 (RIP2) is associated with the malignant character of cancer cells. However, it remains unclear whether RIP2 is involved in TMZ resistance in glioma.
methodsRIP2 expression was inhibited in TMZ-resistant glioma cells and normal glioma cells by using small interfering RNA (siRNA) against RIP2. Plasmid transfection method was used to overexpress RIP2. Cell counting kit-8 assays were performed to evaluate cell viability. Western blotting or immunofluorescence was performed to determine RIP2, NF-κB, and MGMT expression in cells. Flow cytometry was used to investigate cell apoptosis. TMZ-resistant glioma xenograft models were established to evaluate the role of the RIP2/NF-κB/MGMT signaling pathway in drug resistance.
resultsWe observed that RIP2 expression was upregulated in TMZ-resistant glioma cells, whereas silencing of RIP2 expression enhanced cellular sensitivity to TMZ. Similarly, upon the induction of RIP2 overexpression, glioma cells developed resistance to TMZ. The molecular mechanism underlying the process indicated that RIP2 can activate the NF-κB signaling pathway and upregulate the expression of O6-methylguanine-DNA methyltransferase (MGMT), following which the glioma cells develop drug resistance. In the TMZ-resistant glioma xenograft model, treatment with JSH-23 (an NF-κB inhibitor) and lomeguatrib (an MGMT inhibitor) could enhance the sensitivity of the transplanted tumor to TMZ.
conclusionWe report that the RIP2/NF-κB/MGMT signaling pathway is involved in the regulation of TMZ resistance. Interference with NF-κB or MGMT activity could constitute a novel strategy for the treatment of RIP2-positive TMZ-resistant glioma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.