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LncRNA MT1DP promotes cadmium-induced DNA replication stress by inhibiting chromatin recruitment of SMARCAL1
被引:11
作者:

Feng, Wenya
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Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
Univ Chinese Acad Sci, Beijing 100049, Peoples R China Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China

Qi, Zijuan
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Shandong First Med Univ, Affiliated Hosp 1, Dept Orthoped Surg, Jinan 250014, Shandong, Peoples R China Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China

Dong, Zheng
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Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
Univ Chinese Acad Sci, Beijing 100049, Peoples R China Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China

Liu, Wei
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Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
Univ Chinese Acad Sci, Beijing 100049, Peoples R China Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China

Xu, Ming
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Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
Univ Chinese Acad Sci, Beijing 100049, Peoples R China Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China

Gao, Ming
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机构:
Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
Univ Chinese Acad Sci, Beijing 100049, Peoples R China Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China

Liu, Sijin
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h-index: 0
机构:
Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
Univ Chinese Acad Sci, Beijing 100049, Peoples R China Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
机构:
[1] Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China
[2] Univ Chinese Acad Sci, Beijing 100049, Peoples R China
[3] Shandong First Med Univ, Affiliated Hosp 1, Dept Orthoped Surg, Jinan 250014, Shandong, Peoples R China
基金:
中国国家自然科学基金;
关键词:
Cd;
MT1DP;
DNA damage;
ATR;
SMARCAL1;
Replication stress;
GENOME STABILITY;
DAMAGE;
ATR;
REPAIR;
CELLS;
MECHANISMS;
TOXICITY;
PATHWAYS;
CANCER;
D O I:
10.1016/j.scitotenv.2021.151078
中图分类号:
X [环境科学、安全科学];
学科分类号:
08 ;
0830 ;
摘要:
Cadmium (Cd) is a well-known carcinogenic metal and widespread environmental pollutant. The effect of Cdinduced carcinogenesis is partly due to accumulated DNA damage and chromosomal aberrations, but the exact mechanisms underlying the genotoxicity of Cd have not been clearly understood. Here, we found that one long non-coding RNA MT1DP is participated in Cd-induced DNA damage and replication stress. Through analyzing the residents from Cd-contaminated area in Southern China, we found that blood DNA repair genes are down regulated in individuals with high urine Cd values compared to those with low urine Cd values, which contrast to the blood MT1DP levels. Through in vitro experiments, we found that MT1DP promotes Cd-induced DNA damage response, genome instability and replication fork stalling. Mechanically, upon Cd treatment, ATR is activated to enhance HIF-1 alpha expression, which in turn promotes the transcription level of MT1DP. Subsequently MT1DP is recruited on the chromatin and binds to SMARCAL1 to competitive inhibit latter's interaction with RPA complexes, finally leading to increased replication stress and DNA damage. In summary, this study provides clear evidence for the role of epigenetic regulation on the genotoxic effect of Cd, and MT1DP-mediated replication stress may represent a novel mechanism for Cd-induced carcinogenesis. (c) 2021 Elsevier B.V. All rights reserved.
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