AI Article Synopsis
- PRKDC plays a crucial role in the non-homologous end joining pathway for DNA repair, and its dysfunction may indicate how sensitive cancer cells are to radiation.
- The study discovered that high levels of PRKDC are present in lung adenocarcinoma (LUAD) and are associated with poorer patient survival, while lower levels correlate with a more activated immune response in tumors.
- The findings suggest that targeting PRKDC could be a valuable approach in lung cancer treatment, as PRKDC inhibitors show strong anti-tumor effects, especially when combined with cisplatin chemotherapy.
Article Abstract
PRKDC is a key factor involved in the ligation step of the non-homologous end joining pathway. Its dysfunction has proven to be a biomarker for radiosensitivity of cancer cells. However, the prognostic value of PRKDC and its underlying mechanisms have not been clarified yet. In this study, we found that PRKDC overexpressed in lung adenocarcinoma (LUAD) and is significantly related to unfavorable survival, while downregulation of PRKDC is link to inflamed tumor immune signature. Our further in vitro results also showed a potent antitumor efficacy of PRKDC inhibitors alone or combined with cisplatin in human lung cancer cells. This study demonstrated that PRKDC is a potential prognostic biomarker, immunotherapy target, and promising combination candidate for chemotherapy for lung cancer, and highlighted the potential of PRKDC-targeted inhibitors for the treatment of lung cancer.
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| http://dx.doi.org/10.1007/s12033-024-01209-3 | DOI Listing |
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