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Updated: Nov 7, 2025
Visualization of DNA Repair Proteins Interaction by Immunofluorescence
Published on: June 26, 2020
AKR1B10 protects against UVC-induced DNA damage in breast cancer cells
Yuanqing Zeng1,2, Jia Li1, Wangyuan Guo1
1Translational Medicine Institute, The First People's Hospital of Chenzhou, University of South China, Chenzhou 423000, China.
Abstract:
The cellular response to DNA damage is crucial for maintaining the integrity and stability of molecular structure. To maintain genome stability, DNA-damaged cells should be arrested so that mutations can be repaired before replication. Although several key components required for this arrest have been discovered, the majority of the pathways are still unclear. Through a number of assays, including cell viability, colony formation, and apotheosis assay, we found that AKR1B10 protected cells from UVC-induced DNA damage. Surprisingly, UVC-induced γH2AX foci and DNA double-strand breaks in the AKR1B10-overexpressing cells were ∼4-5 folds lower than those in the control group. The expression levels of AKR1B10, p53, chk1, chk2, nuclear factor (NF)-κB, and p65 showed dynamic changes in response to UVC irradiation. Our results suggested that AKR1B10 is involved in the pathway of cell cycle checkpoint and NF-κB in DNA damage. Taken together, our results suggest that AKR1B10 is involved in the repair of the DNA double-strand break, which provides a new insight into the role of AKR1B10 in DNA damage repair and indicates a new trail in tumorigenesis and cancer drug resistance.
Insights
AKR1B10 protects cells from UVC-induced DNA damage by reducing double-strand breaks. This suggests AKR1B10 plays a role in DNA repair, impacting tumorigenesis and cancer drug resistance.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Cellular response to DNA damage is vital for genome stability.
- DNA damage triggers cell cycle arrest for repair before replication.
- Key pathways in DNA damage response are not fully understood.
Purpose of the Study:
- To investigate the role of AKR1B10 in cellular response to UVC-induced DNA damage.
- To elucidate the involvement of AKR1B10 in DNA repair mechanisms.
- To explore the potential implications of AKR1B10 in cancer development and treatment.
Main Methods:
- Cell viability assays
- Colony formation assays
- Apoptosis assays
- Analysis of DNA double-strand breaks (γH2AX foci)
- Western blotting for key proteins (AKR1B10, p53, chk1, chk2, NF-κB, p65)
Main Results:
- AKR1B10 overexpression significantly protected cells against UVC-induced DNA damage.
- UVC-induced γH2AX foci and DNA double-strand breaks were reduced by 4-5 fold in AKR1B10-overexpressing cells.
- Expression levels of AKR1B10, p53, chk1, chk2, and NF-κB signaling components (p65) dynamically changed post-UVC irradiation.
Conclusions:
- AKR1B10 is involved in the cell cycle checkpoint and NF-κB pathways during DNA damage response.
- AKR1B10 plays a role in the repair of DNA double-strand breaks.
- AKR1B10's function in DNA repair offers new insights into tumorigenesis and cancer drug resistance.
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