ArticleOncogene2019
Fstl1/DIP2A/MGMT signaling pathway plays important roles in temozolomide resistance in glioblastoma.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Bibliometric and visualization analysis in the field of epigenetics and glioma (2009-2024).Frontiers in oncology · 2024Pooled it
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- Tetrahedral framework nucleic acids: Nanokeys unlocking a new era of precision biomedicine.Journal of advanced research · 2026Review
- Article
- Acetylation modification in malignant progression and therapeutic resistance of gliomas.Frontiers in cell and developmental biology · 2026Review
- In Lower-Grade Gliomas, the SPARC Family Exacerbates Prognosis by Influencing Immunity, Stemness, and Metabolism.Cancer reports (Hoboken, N.J.) · 2025Article
- Post-translational modifications in DNA damage repair: mechanisms underlying temozolomide resistance in glioblastoma.Oncogene · 2025Review
- Transcriptomic profiling ofComputational and structural biotechnology journal · 2024Article
- Robust self-supervised learning strategy to tackle the inherent sparsity in single-cell RNA-seq data.Briefings in bioinformatics · 2024Article
- MEN1 Deficiency-Driven Activation of the β-Catenin-MGMT Axis Promotes Pancreatic Neuroendocrine Tumor Growth and Confers Temozolomide Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- O-6-Methylguanine-DNA Methyltransferase, C-MYC, and EBER Status in Diffuse Large B-Cell Lymphoma of Central Nervous System.International journal of molecular and cellular medicine · 2024Article
- Prognostic significance of the FSTL1-DIP2A axis in early-stage tongue cancer.American journal of cancer research · 2024Article
- Polydopamine-based loaded temozolomide nanoparticles conjugated by peptide-1 for glioblastoma chemotherapy and photothermal therapy.Frontiers in pharmacology · 2023Article
- An overview of glioblastoma multiforme and temozolomide resistance: can LC-MS-based proteomics reveal the fundamental mechanism of temozolomide resistance?Frontiers in oncology · 2023Review
- Hsa_circ_0058129 regulates papillary thyroid cancer development via miR-873-5p/follistatin-like 1 axis.Journal of clinical laboratory analysis · 2022Article
- Identification of differentially expressed and methylated genes and construction of a co-expression network in age-related macular degeneration.Annals of translational medicine · 2022Article
- The regulatory pattern of target gene expression by aberrant enhancer methylation in glioblastoma.BMC bioinformatics · 2021Article
- Regulation of temozolomide resistance in glioma cells via the RIP2/NF-κB/MGMT pathway.CNS neuroscience & therapeutics · 2021Article
- TGF-β1 modulates temozolomide resistance in glioblastoma via altered microRNA processing and elevated MGMT.Neuro-oncology · 2021Article
- COL5A1 Serves as a Biomarker of Tumor Progression and Poor Prognosis and May Be a Potential Therapeutic Target in Gliomas.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Temozolomide was recognized as the first-line therapy for glioblastoma to prolong the survival of patients noticeably, while recent clinical studies found that some patients were not sensitive to temozolomide treatment. The possible mechanisms seemed to be methylguanine-DNA-methyltransferase (MGMT), mismatch repair, PARP, etc. And the abnormal expression of MGMT might be the most direct factor. In this study, we provide evidence that Fstl1 plays a vital role in temozolomide resistance by sequentially regulating DIP2A protein distribution, H3K9 acetylation (H3K9Ac), and MGMT transcription. As a multifunctional protein widely distributed in cells, DIP2A cooperates with the HDAC2-DMAP1 complex to enhance H3K9Ac deacetylation, prevent MGMT transcription, and increase temozolomide sensitivity. Fstl1, a glycoprotein highly expressed in glioblastoma, competitively binds DIP2A to block DIP2A nuclear translocation, so as to hinder DIP2A from binding the HDAC2-DMAP1 complex. The overexpression of Fstl1 promoted the expression of MGMT in association with increased promoter H3K9Ac. Upregulation of Fstl1 enhanced temozolomide resistance, whereas Fstl1 silencing obviously sensitized GBM cells to temozolomide both in vivo and in vitro. Moreover, DIP2A depletion abolished the effects of Fstl1 on MGMT expression and temozolomide resistance. These findings highlight an important role of Fstl1 in the regulation of temozolomide resistance by modulation of DIP2A/MGMT signaling.
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Registered trials
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.