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• W2904384471 startingPage "317" @default.
• W2904384471 abstract "Radiotherapy is the major treatment modality for malignant glioma. However, the treatment response of radiotherapy is suboptimal due to resistance. Here we aimed to explore the effect and mechanism of Mothers against decapentaplegic homologue (SMAD3) silencing in sensitizing malignant glioma to radiotherapy. Clonogenic assay was used to evaluate the sensitivity of glioma cells to increasing doses of radiation. Glioma cells were transfected with small-interfering RNAs (siRNAs) specific to SMAD3. Overexpression of SMAD3 was achieved by transfecting expression plasmid encoding SMAD3 cDNA. Changes in MRE11-RAD50-NBS1 mRNA and protein levels were assessed through qPCR analysis and western blot analysis, respectively. Chromatin immunoprecipitation (ChIP) was used to confirm the interaction between SMAD3 and MRE11-RAD50-NBS1 (MRN) complex. Silencing of SMAD3 increased sensitivity of glioma cells to radiotherapy. MRE11, RAD50 and NBS1 were overexpressed in response to radiotherapy, which was attenuated by SMAD3 silencing while boosted by SMAD3 overexpression. ChIP analysis confirmed the interaction of SMAD3 with MRE11, RAD50 and NBS1 under radiotherapy, which was inhibited by SMAD3 silencing. SMAD3 silencing is an effective strategy for sensitizing glioma to radiotherapy, which is mediated by the interaction of SMAD3 with the MRN complex." @default.
• W2904384471 created "2018-12-22" @default.
• W2904384471 creator A5004330700 @default.
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• W2904384471 date "2018-12-06" @default.
• W2904384471 modified "2023-09-26" @default.
• W2904384471 title "<i>SMAD3</i>silencing enhances DNA damage in radiation therapy by interacting with<i>MRE11</i>-<i>RAD50</i>-<i>NBS1</i>complex in glioma" @default.
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• W2904384471 doi "https://doi.org/10.1093/jb/mvy110" @default.
• W2904384471 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30535026" @default.
• W2904384471 hasPublicationYear "2018" @default.
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