MicroRNAs, DNA Damage Response, and Cancer Treatment

被引:45
作者
He, Mingyang [1 ]
Zhou, Weiwei [1 ]
Li, Chuang [1 ]
Guo, Mingxiong [1 ]
机构
[1] Wuhan Univ, Coll Life Sci, Hubei Key Lab Cell Homeostasis, Wuhan 430072, Peoples R China
基金
中国国家自然科学基金;
关键词
microRNAs; DNA damage response; DNA repair; radiotherapy; chemotherapy; RADIATION-INDUCED APOPTOSIS; CELL LUNG-CANCER; SCREEN IDENTIFIES MIRNAS; TUMOR-SUPPRESSOR P53; IONIZING-RADIATION; BREAST-CANCER; NEGATIVE REGULATION; GLIOBLASTOMA CELLS; HOMOLOGOUS RECOMBINATION; CISPLATIN RESISTANCE;
D O I
10.3390/ijms17122087
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
As a result of various stresses, lesions caused by DNA-damaging agents occur constantly in each cell of the human body. Generally, DNA damage is recognized and repaired by the DNA damage response (DDR) machinery, and the cells survive. When repair fails, the genomic integrity of the cell is disrupted-a hallmark of cancer. In addition, the DDR plays a dual role in cancer development and therapy. Cancer radiotherapy and chemotherapy are designed to eliminate cancer cells by inducing DNA damage, which in turn can promote tumorigenesis. Over the past two decades, an increasing number of microRNAs (miRNAs), small noncoding RNAs, have been identified as participating in the processes regulating tumorigenesis and responses to cancer treatment with radiation therapy or genotoxic chemotherapies, by modulating the DDR. The purpose of this review is to summarize the recent findings on how miRNAs regulate the DDR and discuss the therapeutic functions of miRNAs in cancer in the context of DDR regulation.
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页数:14
相关论文
共 112 条
[1]   MicroRNA miR-885-5p targets CDK2 and MCM5, activates p53 and inhibits proliferation and survival [J].
Afanasyeva, E. A. ;
Mestdagh, P. ;
Kumps, C. ;
Vandesompele, J. ;
Ehemann, V. ;
Theissen, J. ;
Fischer, M. ;
Zapatka, M. ;
Brors, B. ;
Savelyeva, L. ;
Sagulenko, V. ;
Speleman, F. ;
Schwab, M. ;
Westermann, F. .
CELL DEATH AND DIFFERENTIATION, 2011, 18 (06) :974-984
[2]   E2F1 confers anticancer drug resistance by targeting ABC transporter family members and Bcl-2 via the p73/DNp73-miR-205 circuitry [J].
Alla, Vijay ;
Kowtharapu, Bhavani S. ;
Engelmann, David ;
Emmrich, Stephan ;
Schmitz, Ulf ;
Steder, Marc ;
Puetzer, Brigitte M. .
CELL CYCLE, 2012, 11 (16) :3067-3078
[3]   MicroRNAs: Genomics, biogenesis, mechanism, and function (Reprinted from Cell, vol 116, pg 281-297, 2004) [J].
Bartel, David P. .
CELL, 2007, 131 (04) :11-29
[4]   MiR-338-5p sensitizes glioblastoma cells to radiation through regulation of genes involved in DNA damage response [J].
Besse, Andrej ;
Sana, Jiri ;
Lakomy, Radek ;
Kren, Leos ;
Fadrus, Pavel ;
Smrcka, Martin ;
Hermanova, Marketa ;
Jancalek, Radim ;
Reguli, Stefan ;
Lipina, Radim ;
Svoboda, Marek ;
Slampa, Pavel ;
Slaby, Ondrej .
TUMOR BIOLOGY, 2016, 37 (06) :7719-7727
[5]   MicroRNA functions [J].
Bushati, Natascha ;
Cohen, Stephen M. .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 2007, 23 :175-205
[6]   Human microRNAs are processed from capped, polyadenylated transcripts that can also function as mRNAs [J].
Cai, XZ ;
Hagedorn, CH ;
Cullen, BR .
RNA, 2004, 10 (12) :1957-1966
[7]   Origins and Mechanisms of miRNAs and siRNAs [J].
Carthew, Richard W. ;
Sontheimer, Erik J. .
CELL, 2009, 136 (04) :642-655
[8]   Radiation-induced microRNA: Discovery, Functional Analysis, and Cancer Radiotherapy [J].
Chaudhry, M. Ahmad .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2014, 115 (03) :436-449
[9]   Radiation-Induced Micro-RNA Modulation in Glioblastoma Cells Differing in DNA-Repair Pathways [J].
Chaudhry, M. Ahmad ;
Sachdeva, Harmeet ;
Omaruddin, Romaica A. .
DNA AND CELL BIOLOGY, 2010, 29 (09) :553-561
[10]   Real-Time PCR Analysis of Micro-RNA Expression in Ionizing Radiation-Treated Cells [J].
Chaudhry, M. Ahmad .
CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS, 2009, 24 (01) :49-55