ArticleJournal of cancer research and clinical oncology2015
Knockdown of telomeric repeat binding factor 2 enhances tumor radiosensitivity regardless of telomerase status.
Article in Journal of cancer research and clinical oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- The role of cellular senescence-related genes in ischemia-reperfusion injury and the identification of their biomarkers.Scientific reports · 2026Article
- Telomerase targeting as a therapeutic approach for sensitizing cancer cells to radiotherapy.Molecular biology reports · 2025Review
- Pan‑cancer analysis of the oncogenic role of telomeric repeat binding factor 2 (TERF2) in human tumors and in vitro validation in gastric cancer by TERF2 knockdown.Discover oncology · 2025Article
- Self-Assembled Peptide-Gold Nanoclusters with SiRNA Targeting Telomeric Response to Enhance Radiosensitivity in Lung Cancer Cells.Small science · 2025Article
- Compartmentalization of telomeres through DNA-scaffolded phase separation.Developmental cell · 2022Article
- Abnormal function of telomere protein TRF2 induces cell mutation and the effects of environmental tumor‑promoting factors (Review).Oncology reports · 2021Review
- Effect of therapies-mediated modulation of telomere and/or telomerase on cancer cells radiosensitivity.Oncotarget · 2018Review
- hTERT gene knockdown enhances response to radio- and chemotherapy in head and neck cancer cell lines through a DNA damage pathway modification.Scientific reports · 2018Article
- UBE2D3 gene overexpression increases radiosensitivity of EC109 esophageal cancer cells in vitro and in vivo.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the effects of TRF2 depletion on radiosensitivity in both the telomerase-positive cell lines (A549) and alternative lengthening of telomere (ALT) cell lines (U2OS).
methodsX-ray irradiation was used to establish two radioresistant cancer models (A549R and U2OSR) from A549 and U2OS. Colony formation assay was applied to examine the radiosensitivity of radioresistant A549R and U2OSR cells and TRF2 low-expression cells. Real-time PCR and TeloTAGGG Telomerase PCR ELISA Kit were performed to examine telomere length and telomerase activity separately. γ-H2AX was detected by immunofluorescence to assess the radiation-induced DSBs.
resultsRadioresistant cancer models were established, in which TRF2 was significantly over-expressed. Low expression of TRF2 protein could enhance the radiosensitivity and induce telomere length of A549 and U2OS cell shortening. In A549 cells with TRF2 down-regulated, the telomerase activity was inhibited, too. TRF2 deficiency increases γ-H2AX foci and fails to protect telomere from radiation.
conclusionThe data suggest that TRF2 is a radioresistant protein in A549 and U2OS cells, and could potentially be a target for radiosensitization of both telomerase-positive and ALT cells in radiotherapy.
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