ArticleOncology reports2019
Targeting RAD51 enhances chemosensitivity of adult T‑cell leukemia‑lymphoma cells by reducing DNA double‑strand break repair.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- FOXM1 inhibition primes terminal differentiation of human iPSC-derived hepatocytes.Cell death discovery · 2026Article
- Abemaciclib Inhibits Retinoblastoma Tumor Growth by Targeting CDK1/2.Investigative ophthalmology & visual science · 2026Article
- Targeting the DNA damage response through TBL1X in mantle cell lymphoma.Blood advances · 2025Article
- RAD51 and RAD50 genetic polymorphisms from homologous recombination repair pathway are associated with disease outcomes and organ toxicities in AML.Blood research · 2024Article
- Indigofera suffruticosa aerial parts extract induce G2/M arrest and ATR/CHK1 pathway in Jurkat cells.BMC complementary medicine and therapies · 2024Article
- Exploring homologous recombination repair and base excision repair pathway genes for possible diagnostic markers in hematologic malignancies.Molecular genetics and genomics : MGG · 2023Article
- DNA Damage Response-Related Proteins Are Prognostic for Outcome in Both Adult and Pediatric Acute Myelogenous Leukemia Patients: Samples from Adults and from Children Enrolled in a Children's Oncology Group Study.International journal of molecular sciences · 2023Article
- Studying the DNA damage response pathway in hematopoietic canine cancer cell lines, a necessary step for finding targets to generate new therapies to treat cancer in dogs.Frontiers in veterinary science · 2023Article
- A Pan-Cancer Bioinformatic Analysis of RAD51 Regarding the Values for Diagnosis, Prognosis, and Therapeutic Prediction.Frontiers in oncology · 2022Article
- Checkpoint kinase‑1 inhibition and etoposide exhibit a strong synergistic anticancer effect on chronic myeloid leukemia cell line K562 by impairing homologous recombination DNA damage repair.Oncology reports · 2020Article
- Non-homologous End-joining Genotype, mRNA Expression, and DNA Repair Capacity in Childhood Acute Lymphocytic Leukemia.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RAD51, is a key homologous recombination protein that repairs DNA damage and maintains gene diversity and stability. Previous studies have demonstrated that the over‑expression of RAD51 is associated with chemotherapy resistance of tumor cells to chemotherapy, and enhanced activity of DNA damage repair (DDR) systems contributes to resistance of adult T‑cell leukemia‑lymphoma (ATL) resistance to chemotherapy. Thus, targeting RAD51 is a potential strategy for the sensitization of ATL cells to chemotherapeutic drugs by inducing DNA damage. In general, cells can repair minor DNA damage through DDR; however, serious DNA damage may cause cell toxicity in cells which cannot be restored. In the present, down regulation of RAD51 by shRNA and imatinib sensitized Jurkat cells to etoposide by decreasing the activity of homologous recombination (HR). We found that the suppression of RAD51 by shRNA inhibited tumor cells proliferation and enhanced apoptosis of Jurkat cells after etoposide treatment. Importantly, downregulation of RAD51 by imatinib obviously increased the apoptosis of Jurkat cell after etoposide treatment. These results demonstrated that RAD51 may be of great value to as a novel target for the clinical treatment of adult T‑cell leukemia‑lymphoma (ATL), and it may improve the survival of leukemia patients.
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