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Updated: Jan 9, 2026

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells
Published on: June 9, 2020
IGF1R promotes radiation-induced HSCs activation by regulating DNA-PKcs-mediated DNA damage repair
Jiguo Lin1, Gang Zhao1, Jie Feng1
1NHC Key Laboratory of Radiobiology, College of Public Health, Jilin University, Changchun, China.
Ionizing radiation activates liver cells by promoting DNA repair through insulin-like growth factor 1 receptor (IGF1R) and DNA-PKcs interactions. Inhibiting this pathway may prevent radiation-induced liver fibrosis.
Area of Science:
- Hepatology
- Radiation Oncology
- Molecular Biology
Background:
- Ionizing radiation (IR) can cause liver fibrosis, a serious complication of liver cancer radiotherapy.
- Hepatic stellate cell (HSC) activation is central to IR-induced liver fibrosis.
- The role of insulin-like growth factor 1 receptor (IGF1R) in DNA damage repair and HSC activation is not fully understood.
Purpose of the Study:
- To investigate the mechanism by which IGF1R regulates DNA damage repair in HSCs.
- To explore the role of IGF1R in IR-induced HSC activation.
Main Methods:
- Confirmation of IR-induced HSC activation, DNA damage, and upregulation of IGF1R and DNA-PKcs.
- Investigation of IGF1R-DNA-PKcs interactions in promoting DNA damage repair and HSC activation.
Main Results:
- IR induces HSC activation, DNA damage, and upregulation of IGF1R and DNA-PKcs.
- IGF1R activation/overexpression promotes IR-induced HSC activation and DNA repair via interaction with DNA-PKcs.
- IGF1R nuclear translocation promotes PRKDC transcription, and cytoplasmic interaction with DNA-PKcs facilitates DNA repair.
Conclusions:
- Inhibition of the IGF1R-DNA-PKcs-dependent non-homologous end joining (NHEJ) repair pathway is a potential strategy to prevent IR-induced HSC activation.
- This study elucidates the novel mechanism of IGF1R in mediating IR-induced HSC activation through DNA-PKcs.
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