ArticleOncology letters2021
Elevated XRCC5 expression level can promote temozolomide resistance and predict poor prognosis in glioblastoma.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Preliminary revelation of potential therapeutic targets related to ribosome biogenesis in lung adenocarcinoma based on bioinformatics analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Multi-omics analysis reveals the role of the XRCC gene family in diagnosis, prognosis, and immunity in pan-cancer.Discover oncology · 2026Article
- X-ray cross-complementing family: the bridge linking DNA damage repair and cancer.Journal of translational medicine · 2023Review
- ADAM17 Confers Temozolomide Resistance in Human Glioblastoma Cells and miR-145 Regulates Its Expression.International journal of molecular sciences · 2023Article
- Article
- Label-Free Quantitative Proteomics Analysis of Adriamycin Selected Multidrug Resistant Human Lung Cancer Cells.Biomolecules · 2022Article
- Suppression of OCT-1 in Metastatic Breast Cancer Cells Reduces Tumor Metastatic Potential, Hypoxia Resistance, and Drug Resistance.Life (Basel, Switzerland) · 2022Article
- Identification of an IFN-β-associated gene signature for the prediction of overall survival among glioblastoma patients.Annals of translational medicine · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance and disease recurrence are important contributors for the poor prognosis of glioblastoma multiforme (GBM). Temozolomide (TMZ), the standard chemotherapy for GBM treatment, can methylate DNA and cause the formation of double-strand breaks (DSBs). X-ray repair cross complementing 5 (XRCC5), also known as Ku80 or Ku86, is required for the repair of DSBs. The present study identified novel determinants that sensitize cells to TMZ, using an array-based short hairpin (sh)RNA library. Then, cBioportal, Oncomine, and R2 databases were used to analyze the association between gene expression levels and clinical characteristics. Subsequently, lentiviral shRNA or pCMV was used to knockdown or overexpress the gene of interest, and the effects on TMZ sensitivity were determined using a MTT assay and western blot analysis. TMZ-resistant cells were also established and were used in
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