Silencing of Insulin-like Growth Factor-1 Receptor Enhances the Radiation Sensitivity of Human Esophageal Squamous Cell Carcinoma in Vitro and in Vivo
Overview
Oncology
Authors
Affiliations
Background: Esophageal squamous cell carcinoma (ESCC) is a prevalent fatal cancer worldwide, and the number of deaths due to this disease is increasing. Due to ESCC resistance to chemotherapy and radiation treatment, new therapies are urgently needed for the improvement of ESCC patient clinical outcomes.
Methods: Eca-109 and TE-1 cells were transfected with 100 nM IGF-1r siRNA, and a combination of IGF-1r siRNA and radiation therapy was tested in vitro and in vivo. The effects of IGF-1r siRNA were determined through Western blotting and flow cytometry experiments.
Results: After radiotherapy, the number of IGF-1r siRNA-transfected Eca-109 cells decreased by approximately 67.3%, and a 78.9% reduction was observed in the transfected TE-1 cells. In addition, the Eca-109 and TE-1 cells that were irradiated following IGF-1r knockdown contained 16.2% and 20.3% apoptotic cells, respectively.
Conclusions: The results of the current study suggest that IGF-1r knockdown may enhance the radiation sensitivity of ESCC and increase the therapeutic effects of radiation both in vitro and in vivo. These results provide strong evidence that the targeted application of siRNA will enable the development of new therapeutic strategies for the clinical treatment of ESCC patients.
An L, Li M, Jia Q Mol Cancer. 2023; 22(1):140.
PMID: 37598158 PMC: 10439611. DOI: 10.1186/s12943-023-01839-2.
Wang H, Wang F, Ouyang W, Jiang X, Li W Oncol Lett. 2020; 20(1):173-182.
PMID: 32565945 PMC: 7285813. DOI: 10.3892/ol.2020.11551.
Therapeutic Targeting of the IGF Axis.
Osher E, Macaulay V Cells. 2019; 8(8).
PMID: 31416218 PMC: 6721736. DOI: 10.3390/cells8080895.
Targeting DNA Double-Strand Break Repair Pathways to Improve Radiotherapy Response.
Toulany M Genes (Basel). 2019; 10(1).
PMID: 30621219 PMC: 6356315. DOI: 10.3390/genes10010025.
Liu X, Chen H, Xu X, Ye M, Cao H, Xu L Oncol Lett. 2018; 16(1):1332-1340.
PMID: 30061953 PMC: 6063047. DOI: 10.3892/ol.2018.8705.