ArticleNeuro-oncology2018
CUX1 stimulates APE1 enzymatic activity and increases the resistance of glioblastoma cells to the mono-alkylating agent temozolomide.
Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Non-coding RNAs-mediated regulation of the MAPK pathway in gastric cancer: translational perspectives.Discover oncology · 2025Review
- Role and mechanism of RPA1 in the development and progression of glioma.Experimental and therapeutic medicine · 2025Article
- The function of MYC in base excision repair protects against RAS-induced senescence.Nucleic acids research · 2025Article
- Protein-Protein Interactions in Base Excision Repair.Biomolecules · 2025Review
- p200CUX1-regulated BMP8B inhibits the progression of acute myeloid leukemia via the MAPK signaling pathway.Medical oncology (Northwood, London, England) · 2024Article
- The function of BCL11B in base excision repair contributes to its dual role as an oncogene and a haplo-insufficient tumor suppressor gene.Nucleic acids research · 2024Article
- Cut homeodomain transcription factor is a novel regulator of growth and morphogenesis of cortex glia niche around neural cells.Genetics · 2024Article
- CUT homeobox genes: transcriptional regulation of neuronal specification and beyond.Frontiers in cellular neuroscience · 2023Review
- The DNA repair function of BCL11A suppresses senescence and promotes continued proliferation of triple-negative breast cancer cells.NAR cancer · 2022Article
- Base excision repair accessory factors in senescence avoidance and resistance to treatments.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- The base excision repair process: comparison between higher and lower eukaryotes.Cellular and molecular life sciences : CMLS · 2021Review
- CUT Domain Proteins in DNA Repair and Cancer.Cancers · 2021Review
- Splicing machinery dysregulation drives glioblastoma development/aggressiveness: oncogenic role of SRSF3.Brain : a journal of neurology · 2020Article
- PARP inhibition suppresses the emergence of temozolomide resistance in a model system.Journal of neuro-oncology · 2020Article
- The splicing component ISY1 regulates APE1 in base excision repair.DNA repair · 2020Article
- CUX1, A Controversial Player in Tumor Development.Frontiers in oncology · 2020Review
- Upregulated Expression of CUX1 Correlates with Poor Prognosis in Glioma Patients: a Bioinformatic Analysis.Journal of molecular neuroscience : MN · 2019Article
- Distinct clinical and biological implications ofBlood advances · 2019Article
- Novel Function of lncRNA ADAMTS9-AS2 in Promoting Temozolomide Resistance in Glioblastoma via Upregulating the FUS/MDM2 Ubiquitination Axis.Frontiers in cell and developmental biology · 2019Article
- CUX2 functions as an oncogene in papillary thyroid cancer.OncoTargets and therapy · 2019Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cut Like homeobox 1 (CUX1), which encodes an auxiliary factor in base excision repair, resides on 7q22.1, the most frequently and highly amplified chromosomal region in glioblastomas. The resistance of glioblastoma cells to the mono-alkylating agent temozolomide is determined to some extent by the activity of apurinic/apyrimidinic endonuclease 1 (APE1). Methods: To monitor the effect of CUX1 and its CUT domains on APE1 activity, DNA repair assays were performed with purified proteins and cell extracts. CUX1 protein expression was analyzed by immunohistochemistry using a tumor microarray of 150 glioblastoma samples. The effect of CUX1 knockdown and overexpression on the resistance of glioblastoma cell lines to temozolomide was investigated. Results: We show that CUT domains stimulate APE1 activity. In agreement with these findings, CUX1 knockdown causes an increase in the number of abasic sites in genomic DNA and a decrease in APE1 activity as measured in cell extracts. Conversely, ectopic CUX1 expression increases APE1 activity and lowers the number of abasic sites. Having established that CUX1 is expressed at high levels in most glioblastomas, we next show that the resistance of glioblastoma cells to temozolomide and to a combined treatment of temozolomide and ionizing radiation is reduced following CUX1 knockdown, but increased by overexpression of CUX1 or a short protein containing only 2 CUT domains, which is active in DNA repair but devoid of transcriptional activity. Conclusion: These findings indicate that CUX1 expression level impacts on the response of glioblastoma cells to treatment and identifies the CUT domains as potential therapeutic targets.
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