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AKR1B10 protects against UVC-induced DNA damage in breast cancer cells.

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收录情况: ◇ SCIE ◇ 统计源期刊 ◇ CSCD-C ◇ 卓越:梯队期刊

机构: [1]Translational Medicine Institute, The First People’s Hospital of Chenzhou, University of South China, Chenzhou 423000, China, [2]Department of Clinical Laboratory, Zhuhai Hospital, Guangdong Hospital of Traditional Chinese Medicine, Zhuhai 519015, China, [3]Affiliated Foshan Maternity & Child Healthcare Hospital, Southern Medical University, Foshan 528000, China, [4]School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 520150, China, [5]Department of Laboratory Medicine, Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), Shenzhen 518000, China, [6]Center for Laboratory and Pathology, National & Local Joint Engineering Laboratory for High-through Molecular Diagnosis Technology, The First People’s Hospital of Chenzhou, Southern Medical University, Chenzhou 423000, China
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关键词: AKR1B10 DNA damage UVC cell cycle checkpoint NF-κB

摘要:
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. © The Author(s) 2021. Published by Oxford University Press on behalf of the Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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出版当年[2020]版:
大类 | 2 区 生物
小类 | 2 区 生物物理 3 区 生化与分子生物学
最新[2025]版:
大类 | 2 区 生物学
小类 | 2 区 生化与分子生物学 2 区 生物物理
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出版当年[2019]版:
Q2 BIOPHYSICS Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
最新[2023]版:
Q1 BIOPHYSICS Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2019版] 出版当年五年平均 出版前一年[2018版] 出版后一年[2020版]

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第一作者机构: [1]Translational Medicine Institute, The First People’s Hospital of Chenzhou, University of South China, Chenzhou 423000, China, [2]Department of Clinical Laboratory, Zhuhai Hospital, Guangdong Hospital of Traditional Chinese Medicine, Zhuhai 519015, China,
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通讯机构: [3]Affiliated Foshan Maternity & Child Healthcare Hospital, Southern Medical University, Foshan 528000, China, [4]School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 520150, China, [5]Department of Laboratory Medicine, Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), Shenzhen 518000, China, [6]Center for Laboratory and Pathology, National & Local Joint Engineering Laboratory for High-through Molecular Diagnosis Technology, The First People’s Hospital of Chenzhou, Southern Medical University, Chenzhou 423000, China
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