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Malignant Transformation - OSTI GOV

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Last Updated: 11 February 2022

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CRL4ADTL degrades DNA-PKcs to modulate NHEJ repair and induce genomic instability and subsequent malignant transformation

One of the key causes of malignant transformation and tumorigenesis is genomic instability induced by DNA damage and inadequate DNA repair. DNA double strand breaks are the most damaging form of DNA damage, and nonhomologous end-joining techniques play primary and priority roles in initiating DSB reconstruction. According to DNA databases, a well-studied oncogene, the ubiquitin ligase Cullin 4A, is expected to be recruited to DSB sites in genomic DNA, but it is uncertain if it regulates NHEJ mechanisms of repair. Here, we discovered that the CUL4A-DTL ligase complex in the NHEJ repair pathway for nuclear destruction attacked the DNA-PKcs protein. CUL4A expression gradually increased with increasing malignant tendency and was positively linked to DNA-PKcs and positively correlated with Î3-H2AX expression, according to a correlated study with Î3-H2AX expression in human precancerous lesions, consistent with the in vitro results. These results also showed that CUL4A might be a prognostic marker of precancerous lesions and a potential cancer treatment target in cancer.

Source link: https://www.osti.gov/biblio/1816055

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions