ArticleMolecular medicine reports2017
ATM mediates DAB2IP-deficient bladder cancer cell resistance to ionizing radiation through the p38MAPK and NF-κB signaling pathway.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
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- Targeting oncogene and non-oncogene addiction to inflame the tumour microenvironment.Nature reviews. Drug discovery · 2022Review
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- Molecular mechanisms of chemo- and radiotherapy resistance and the potential implications for cancer treatment.MedComm · 2021Review
- Immunological impact of cell death signaling driven by radiation on the tumor microenvironment.Nature immunology · 2020Review
- Predictive and Prognostic Value of DNA Damage Response Associated Kinases in Solid Tumors.Frontiers in oncology · 2020Review
- Antrocin Sensitizes Prostate Cancer Cells to Radiotherapy through Inhibiting PI3K/AKT and MAPK Signaling Pathways.Cancers · 2018Article
- Potential roles of reactive oxygen species derived from chemical substances involved in cancer development in the female reproductive system.BMB reports · 2018Review
- Role of the NFκB-signaling pathway in cancer.OncoTargets and therapy · 2018Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although surgery remains the standard therapy for the treatment of bladder cancer (BCa), the data from previous clinical studies suggest that there is an increase in the number of patients with a preference for bladder preservation strategies, including radiotherapy, to improve their life quality. Our preliminary results showed that disabled homolog 2 interactive protein (DAB2IP), a putative tumor suppressor gene, is often downregulated in BCa with a radioresistant phenotype. Subsequent investigations revealed that elevated expression of ataxia‑telangiectasia mutated (ATM) induced by DAB2IP‑knockdown may be the key event in BCa cell resistance to ionizing radiation (IR). However, how ATM is involved in the survival of DAB2IP‑deficient cells exposed to IR remains to be fully elucidated. The present study knocked down the expression of ATM in DAB2IP‑deficient BCa cells using RNA interference technology. Activation of mitogen‑activated protein kinase (MAPK) and nuclear factor‑κB (NF‑κB) signaling pathways were detected by western blot analysis and immunofluorescence assay, respectively. It was demonstrated that knockdown of ATM enhanced the response of DAB2IP‑deficient BCa cells to IR, which may have resulted from delayed DNA double‑strand break repair kinetics, compromised nuclear factor‑κB translocation, inhibited phosphorylation of p38 and the induced activation of c‑Jun N‑terminal kinase. Taken together, these findings suggested that ATM may be an effective target in the radiotherapy of patients with DAB2IP-deficient BCa.
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