ArticleOncoTargets and therapy2020
End Processing Factor APLF Promotes NHEJ Efficiency and Contributes to TMZ- and Ionizing Radiation-Resistance in Glioblastoma Cells.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- BARD1: A Friend or Foe in Pancreatic Ductal Adenocarcinoma?International journal of molecular sciences · 2025Review
- MST1 enhances radio-sensitivity in glioblastoma by suppressing autophagy and promoting apoptosis.American journal of cancer research · 2025Article
- Comparative Review on Cancer Pathology from Aberrant Histone Chaperone Activity.International journal of molecular sciences · 2024Review
- DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy.Signal transduction and targeted therapy · 2021Review
- XPA Enhances Temozolomide Resistance of Glioblastoma Cells by Promoting Nucleotide Excision Repair.Cell transplantationArticle
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeGlioblastoma (GBM) is the most commonly diagnosed primary brain tumor in adults. Despite a variety of advances in the understanding of GBM cancer biology during recent decades, very few of them were applied into treatment, and the survival rate of GBM patients has not been improved majorly due to the low chemosensitivity to temozolomide (TMZ) or low radiosensitivity. Therefore, it is urgent to elucidate mechanisms of TMZ- and IR-resistance and develop novel therapeutic strategies to improve GBM treatment.
methodsTMZ- and IR-resistant cell lines were acquired by continuous exposing parental GBM cells to TMZ or IR for 3 months. Cell viability was determined by using Sulforhodamine B (SRB) assay. Protein and mRNA expression were examined by Western blotting assay and quantitative polymerase chain reaction (qPCR) assay, respectively. Homologous recombination (HR) and nonhomologous end joining (NHEJ) efficiency were measured by HR and NHEJ reporter assay. Cell apoptosis was determined by Caspase3/7 activity. Autophagy was analyzed using CYTO-ID
resultsDNA repair efficiency of non-homologous end joining (NHEJ) pathway is significantly increased in TMZ- and IR-resistant GBM cells. Importantly, APLF, which is one of the DNA end processing factors in NHEJ, is upregulated in TMZ- and IR-resistant GBM cells and patients. APLF deficiency significantly decreases NHEJ efficiency and improves cell sensitivity to TMZ and IR both in vitro and in vivo.
conclusionOur study provides evidence for APLF serving as a promising, novel target in GBM chemo- and radio-therapy.
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