MiR-1587 Regulates DNA Damage Repair and the Radiosensitivity of CRC Cells via Targeting LIG4

DNA is subject to a range of endogenous and exogenous insults that can impair DNA replication and lead to DNA double-strand breaks (DSBs). The repair capacity of cancer cells mediates their radiosensitivity, but the roles of miR-1587 during radiation resistance are poorly characterized. In this stud...

Full description

Saved in:
Bibliographic Details
Published in:Dose-response Vol. 18; no. 2; p. 155932582093690
Main Authors: Liu, Ruixue, Shen, Liping, Lin, Chuxian, He, Junyan, Wang, Qi, Qi, Zhenhua, Zhang, Qingtong, Zhou, Meijuan, Wang, Zhidong
Format: Journal Article
Language:English
Published: Los Angeles, CA SAGE Publications 01.04.2020
SAGE PUBLICATIONS, INC
SAGE Publishing
Subjects:
ISSN:1559-3258, 1559-3258
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Abstract DNA is subject to a range of endogenous and exogenous insults that can impair DNA replication and lead to DNA double-strand breaks (DSBs). The repair capacity of cancer cells mediates their radiosensitivity, but the roles of miR-1587 during radiation resistance are poorly characterized. In this study, we explored whether miR-1587 regulates the growth and radiosensitivity of colorectal cancer (CRC) cells through its ability to regulate DNA Ligase4 (LIG4). We found that CRC cells in which miR-1587 was overexpressed inhibited cell growth and promoted apoptosis through increasing DSBs and promoting cell cycle arrest. We found that overexpression of miR-1587 significantly inhibited LIG4 messenger RNA and protein expression and further revealed the ability of miR-1587 to directly bind to the LIG4-3′-untranslated region through dual-luciferase reporter assays. More notably, miR-1587 mimics increased the radiosensitivity of CRC cells. Taken together, we show that miR-1587 overexpression enhances the formation of DSBs, arrests CRC cell growth, and enhances the radiosensivity of CRC cells through the direct repression of LIG4 expression. These results reveal novel roles for miR-1587 during DNA damage repair and the radiosensivity of CRC cells. This highlights miR-1587 as a novel therapeutic target for CRC.
AbstractList DNA is subject to a range of endogenous and exogenous insults that can impair DNA replication and lead to DNA double-strand breaks (DSBs). The repair capacity of cancer cells mediates their radiosensitivity, but the roles of miR-1587 during radiation resistance are poorly characterized. In this study, we explored whether miR-1587 regulates the growth and radiosensitivity of colorectal cancer (CRC) cells through its ability to regulate DNA Ligase4 (LIG4). We found that CRC cells in which miR-1587 was overexpressed inhibited cell growth and promoted apoptosis through increasing DSBs and promoting cell cycle arrest. We found that overexpression of miR-1587 significantly inhibited LIG4 messenger RNA and protein expression and further revealed the ability of miR-1587 to directly bind to the LIG4-3'-untranslated region through dual-luciferase reporter assays. More notably, miR-1587 mimics increased the radiosensitivity of CRC cells. Taken together, we show that miR-1587 overexpression enhances the formation of DSBs, arrests CRC cell growth, and enhances the radiosensivity of CRC cells through the direct repression of LIG4 expression. These results reveal novel roles for miR-1587 during DNA damage repair and the radiosensivity of CRC cells. This highlights miR-1587 as a novel therapeutic target for CRC.DNA is subject to a range of endogenous and exogenous insults that can impair DNA replication and lead to DNA double-strand breaks (DSBs). The repair capacity of cancer cells mediates their radiosensitivity, but the roles of miR-1587 during radiation resistance are poorly characterized. In this study, we explored whether miR-1587 regulates the growth and radiosensitivity of colorectal cancer (CRC) cells through its ability to regulate DNA Ligase4 (LIG4). We found that CRC cells in which miR-1587 was overexpressed inhibited cell growth and promoted apoptosis through increasing DSBs and promoting cell cycle arrest. We found that overexpression of miR-1587 significantly inhibited LIG4 messenger RNA and protein expression and further revealed the ability of miR-1587 to directly bind to the LIG4-3'-untranslated region through dual-luciferase reporter assays. More notably, miR-1587 mimics increased the radiosensitivity of CRC cells. Taken together, we show that miR-1587 overexpression enhances the formation of DSBs, arrests CRC cell growth, and enhances the radiosensivity of CRC cells through the direct repression of LIG4 expression. These results reveal novel roles for miR-1587 during DNA damage repair and the radiosensivity of CRC cells. This highlights miR-1587 as a novel therapeutic target for CRC.
DNA is subject to a range of endogenous and exogenous insults that can impair DNA replication and lead to DNA double-strand breaks (DSBs). The repair capacity of cancer cells mediates their radiosensitivity, but the roles of miR-1587 during radiation resistance are poorly characterized. In this study, we explored whether miR-1587 regulates the growth and radiosensitivity of colorectal cancer (CRC) cells through its ability to regulate DNA Ligase4 (LIG4). We found that CRC cells in which miR-1587 was overexpressed inhibited cell growth and promoted apoptosis through increasing DSBs and promoting cell cycle arrest. We found that overexpression of miR-1587 significantly inhibited LIG4 messenger RNA and protein expression and further revealed the ability of miR-1587 to directly bind to the LIG4-3′-untranslated region through dual-luciferase reporter assays. More notably, miR-1587 mimics increased the radiosensitivity of CRC cells. Taken together, we show that miR-1587 overexpression enhances the formation of DSBs, arrests CRC cell growth, and enhances the radiosensivity of CRC cells through the direct repression of LIG4 expression. These results reveal novel roles for miR-1587 during DNA damage repair and the radiosensivity of CRC cells. This highlights miR-1587 as a novel therapeutic target for CRC.
Author Zhou, Meijuan
Qi, Zhenhua
Wang, Qi
Zhang, Qingtong
Wang, Zhidong
He, Junyan
Liu, Ruixue
Shen, Liping
Lin, Chuxian
AuthorAffiliation 2 Department of Radiobiology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, People’s Republic of China
1 Department of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, People’s Republic of China
3 Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, People’s Republic of China
AuthorAffiliation_xml – name: 2 Department of Radiobiology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, People’s Republic of China
– name: 1 Department of Radiation Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, People’s Republic of China
– name: 3 Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, People’s Republic of China
Author_xml – sequence: 1
  givenname: Ruixue
  surname: Liu
  fullname: Liu, Ruixue
– sequence: 2
  givenname: Liping
  surname: Shen
  fullname: Shen, Liping
– sequence: 3
  givenname: Chuxian
  surname: Lin
  fullname: Lin, Chuxian
– sequence: 4
  givenname: Junyan
  surname: He
  fullname: He, Junyan
– sequence: 5
  givenname: Qi
  surname: Wang
  fullname: Wang, Qi
  email: wangzhidong_1977@aliyun.com
– sequence: 6
  givenname: Zhenhua
  surname: Qi
  fullname: Qi, Zhenhua
– sequence: 7
  givenname: Qingtong
  surname: Zhang
  fullname: Zhang, Qingtong
– sequence: 8
  givenname: Meijuan
  surname: Zhou
  fullname: Zhou, Meijuan
– sequence: 9
  givenname: Zhidong
  surname: Wang
  fullname: Wang, Zhidong
  email: wangzhidong_1977@aliyun.com
BookMark eNp9Uk1v1DAUjFAR_YA7R0tcuAT8ETvOBalKS7vSAtKqHJH1nNipV9l4sb0r9d_jsK2gK8HJ9ryZsd_4nRcnk59MUbwl-AMhdf2RcN4wyiXFDRMNFi-KsxkqZ-zkr_1pcR7jGuOK14y8Kk4ZFUzUlJ4VP764VUm4rNHKDLsRkono6usluoINDCaDW3ABwdSjdJ-P0DsfzRRdcnuXHpC3qF21qDXjGNHeAbqDMJjkpgEtFzfV6-KlhTGaN4_rRfH98_Vde1suv90s2stl2XHMUwm9JabhFKxkNRABTDIr-kpCxbAGanDfadoziQEL4I02uoHGMt1ZKjQIdlEsDr69h7XaBreB8KA8OPUb8GFQEJLrRqNwpWmNrW6sJhXBtayF0doSKmUjKw3Z69PBa7vTG9N3ZkoBxmemzyuTu1eD36scLReSZ4P3jwbB_9yZmNTGxS4nBJPxu6hoRUmV8yckU98dUdd-F6Yc1czimBDCcWaJA6sLPsZgrOpcguT8fL8bFcFqngZ1PA1ZiI-ET138R1IeJDF__5_X_JP_C0btwQk
CitedBy_id crossref_primary_10_3233_THC_230453
crossref_primary_10_1016_j_hermed_2024_100934
crossref_primary_10_1016_j_procbio_2023_05_004
crossref_primary_10_1080_09205063_2024_2346395
crossref_primary_10_1016_j_biopha_2023_114485
crossref_primary_10_1016_j_currproblcancer_2023_101036
crossref_primary_10_3390_ijms23063231
crossref_primary_10_1016_j_ajg_2023_02_001
crossref_primary_10_2217_pgs_2022_0121
crossref_primary_10_1016_j_lfs_2020_119005
crossref_primary_10_1159_000537819
crossref_primary_10_3892_ol_2022_13390
crossref_primary_10_1016_j_ijbiomac_2023_123279
crossref_primary_10_3389_fonc_2022_889658
Cites_doi 10.1038/nrm1202
10.1126/scitranslmed.aac5671
10.1038/nrd.2016.246
10.1016/j.suronc.2012.03.004
10.1158/0008-5472.CAN-14-2783
10.1158/0008-5472.CAN-16-3105
10.1016/j.cels.2017.09.015
10.1038/cddis.2013.171
10.1016/j.cell.2012.04.005
10.1158/1078-0432.CCR-07-5147
10.1038/nrg3765
10.1038/nrc3107
10.18632/aging.100998
10.1158/1078-0432.CCR-14-0326
10.1159/000491532
10.1517/14712598.2014.950650
10.1158/2159-8290.CD-15-0893
10.1146/annurev-med-081313-121208
10.1016/j.dnarep.2004.03.025
10.1074/jbc.TM117.000374
10.15252/embj.201797651
10.1074/jbc.M116.772392
10.1038/s41590-019-0336-y
10.1038/nature08467
10.1038/nrd4359
10.1038/s41416-018-0192-9
10.1016/j.celrep.2017.08.091
10.1101/gr.082701.108
10.1016/j.tibs.2011.06.002
10.1053/j.gastro.2015.05.057
10.1016/j.semcancer.2016.02.002
10.1097/DCR.0000000000000742
10.1093/nar/gkv273
ContentType Journal Article
Copyright The Author(s) 2020
The Author(s) 2020. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
The Author(s) 2020.
The Author(s) 2020 2020 SAGE Publications
Copyright_xml – notice: The Author(s) 2020
– notice: The Author(s) 2020. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: The Author(s) 2020.
– notice: The Author(s) 2020 2020 SAGE Publications
DBID AFRWT
AAYXX
CITATION
3V.
7X7
7XB
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BENPR
CCPQU
DWQXO
FYUFA
GHDGH
K9.
M0S
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
PRINS
7X8
5PM
DOA
DOI 10.1177/1559325820936906
DatabaseName Sage Journals GOLD Open Access 2024
CrossRef
ProQuest Central (Corporate)
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
ProQuest Central
ProQuest One
ProQuest Central
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Health & Medical Complete (Alumni)
ProQuest Health & Medical Collection
ProQuest Central Premium
ProQuest One Academic (New)
Publicly Available Content Database
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic (retired)
ProQuest One Academic UKI Edition
ProQuest Central China
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest One Academic Eastern Edition
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest One Health & Nursing
ProQuest Central China
ProQuest Hospital Collection (Alumni)
ProQuest Central
ProQuest Health & Medical Complete
ProQuest Health & Medical Research Collection
Health Research Premium Collection
ProQuest One Academic UKI Edition
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
ProQuest Central (New)
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList MEDLINE - Academic
Publicly Available Content Database


CrossRef

Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: PIMPY
  name: Publicly Available Content Database
  url: http://search.proquest.com/publiccontent
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Public Health
EISSN 1559-3258
ExternalDocumentID oai_doaj_org_article_04b270fb9fb14107876ebbf1288984ba
PMC7315685
10_1177_1559325820936906
10.1177_1559325820936906
GroupedDBID ---
0R~
29G
2WC
53G
54M
5GY
5VS
7X7
8FI
8FJ
AAFWJ
AAJPV
AAJQC
AAKDD
AAQQG
AASGM
ABAWP
ABDBF
ABJIS
ABNCE
ABQXT
ABUWG
ABVFX
ABXGC
ACARO
ACDXX
ACGFS
ACROE
ACUHS
ADBBV
ADOGD
AENEX
AEUHG
AEWDL
AFCOW
AFKRA
AFKRG
AFPKN
AFRWT
AJUZI
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AOIJS
ARTOV
AUTPY
AYAKG
B0M
BAWUL
BCNDV
BDDNI
BENPR
BPHCQ
BSEHC
BVXVI
CCPQU
CS3
DC.
DIK
DU5
E3Z
EAP
EBD
EBS
EDH
EMK
ESX
FYUFA
GROUPED_DOAJ
GX1
H13
HMCUK
HYE
J8X
K.F
KQ8
MET
MK0
M~E
O9-
PHGZM
PHGZT
PIMPY
PQQKQ
ROL
RPM
SAUOL
SCDPB
SCNPE
SFC
TR2
TUS
UKHRP
~8M
AAYXX
ACHEB
AFFHD
BANNL
CITATION
3V.
7XB
8FK
AZQEC
DWQXO
K9.
PJZUB
PKEHL
PPXIY
PQEST
PQUKI
PRINS
7X8
PUEGO
5PM
ID FETCH-LOGICAL-c505t-adf1e952af837a16a383f6d48a430ba2e0dcb2d380a06a59beb9a9f3bcf26ba63
IEDL.DBID BENPR
ISICitedReferencesCount 18
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000545657000001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 1559-3258
IngestDate Mon Nov 10 04:33:05 EST 2025
Tue Nov 04 01:55:24 EST 2025
Wed Oct 01 13:54:12 EDT 2025
Tue Oct 07 06:57:31 EDT 2025
Tue Nov 18 22:43:36 EST 2025
Sat Nov 29 08:10:08 EST 2025
Tue Jun 17 22:31:03 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 2
Keywords LIG4
DNA double-strand breaks
radiosensitivity
miR-1587
Language English
License This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c505t-adf1e952af837a16a383f6d48a430ba2e0dcb2d380a06a59beb9a9f3bcf26ba63
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
OpenAccessLink https://www.proquest.com/docview/2425011150?pq-origsite=%requestingapplication%
PMID 32636722
PQID 2425011150
PQPubID 4450826
ParticipantIDs doaj_primary_oai_doaj_org_article_04b270fb9fb14107876ebbf1288984ba
pubmedcentral_primary_oai_pubmedcentral_nih_gov_7315685
proquest_miscellaneous_2421463611
proquest_journals_2425011150
crossref_citationtrail_10_1177_1559325820936906
crossref_primary_10_1177_1559325820936906
sage_journals_10_1177_1559325820936906
PublicationCentury 2000
PublicationDate 2020-04-01
PublicationDateYYYYMMDD 2020-04-01
PublicationDate_xml – month: 04
  year: 2020
  text: 2020-04-01
  day: 01
PublicationDecade 2020
PublicationPlace Los Angeles, CA
PublicationPlace_xml – name: Los Angeles, CA
– name: Thousand Oaks
– name: Sage CA: Los Angeles, CA
PublicationTitle Dose-response
PublicationYear 2020
Publisher SAGE Publications
SAGE PUBLICATIONS, INC
SAGE Publishing
Publisher_xml – name: SAGE Publications
– name: SAGE PUBLICATIONS, INC
– name: SAGE Publishing
References Nikitaki, Mavragani, Laskaratou 2016; 37-38
Friedman, Farh, Burge, Bartel 2008; 19
Lee, Park, Jeong 2015; 75
Hu, Wang, Hu 2017; 292
Pannunzio, Watanabe, Lieber 2018; 293
Tarish, Schultz, Tanoglidi 2015; 7
Rube, Grudzenski, Kuhne 2008; 14
Mo, Song, Huang 2018; 119
Goldstein, Kastan 2015; 66
Conlin, Reid, Small 2017; 20
O Driscoll, Gennery, Seidel, Concannon, Jeggo 2004; 3
Polytarchou, Hommes, Palumbo 2015; 149
Barshishat, Elgrably-Weiss, Edelstein 2018; 37
Chao, Poovey, Privette 2017; 5
Rupaimoole, Slack 2017; 16
Wan, Mathur, Hu, Zhang, Lu 2011; 36
Thangavel, Boopathi, Ciment 2014; 20
Jiang, Shen, Fei 2013; 4
Baker, Salameh, Al-Salman, Daoud 2012; 21
Zhang, Zhang, Li, Zhang, Zhang 2018; 47
Ebert, Sharp 2012; 149
Jackson, Bartek 2009; 461
Cameron, Castoldi, Sanin 2019; 20
van Kouwenhove, Kedde, Agami 2011; 11
Pajic, Froio, Daly 2018; 78
He, Lin, Tang 2016; 8
Li, Rana 2014; 13
Rupaimoole, Calin, Lopez-Berestein, Sood 2016; 6
Hatano, Kumar, Zhang 2015; 43
Kawai, Ishihara, Nozawa 2017; 60
Bottai, Pasculli, Calin, Santarpia 2014; 14
Lieber, Ma, Pannicke, Schwarz 2003; 4
Hausser, Zavolan 2014; 15
bibr9-1559325820936906
bibr21-1559325820936906
bibr13-1559325820936906
bibr4-1559325820936906
bibr26-1559325820936906
bibr12-1559325820936906
bibr18-1559325820936906
bibr27-1559325820936906
bibr33-1559325820936906
bibr14-1559325820936906
bibr20-1559325820936906
bibr5-1559325820936906
bibr1-1559325820936906
bibr6-1559325820936906
bibr11-1559325820936906
bibr32-1559325820936906
bibr19-1559325820936906
bibr15-1559325820936906
bibr2-1559325820936906
bibr10-1559325820936906
bibr28-1559325820936906
bibr23-1559325820936906
bibr24-1559325820936906
bibr7-1559325820936906
bibr29-1559325820936906
bibr16-1559325820936906
bibr31-1559325820936906
bibr8-1559325820936906
bibr22-1559325820936906
bibr3-1559325820936906
bibr25-1559325820936906
bibr17-1559325820936906
bibr30-1559325820936906
References_xml – volume: 119
  start-page: 492
  issue: 4
  year: 2018
  end-page: 502
  article-title: Exosome-packaged miR-1246 contributes to bystander DNA damage by targeting LIG4
  publication-title: Br J Cancer
– volume: 15
  start-page: 599
  issue: 9
  year: 2014
  end-page: 612
  article-title: Identification and consequences of miRNA–target interactions—beyond repression of gene expression
  publication-title: Nat Rev Genet
– volume: 149
  start-page: 981
  issue: 4
  year: 2015
  end-page: 992
  article-title: MicroRNA214 is associated with progression of ulcerative colitis, and inhibition reduces development of colitis and colitis-associated cancer in mice
  publication-title: Gastroenterology
– volume: 7
  start-page: 311r
  issue: 312
  year: 2015
  end-page: 312r
  article-title: Castration radiosensitizes prostate cancer tissue by impairing DNA double-strand break repair
  publication-title: Sci Transl Med
– volume: 43
  start-page: 4075
  issue: 8
  year: 2015
  end-page: 4086
  article-title: A functional screen identifies miRNAs that inhibit DNA repair and sensitize prostate cancer cells to ionizing radiation
  publication-title: Nucleic Acids Res
– volume: 75
  start-page: 1298
  issue: 7
  year: 2015
  end-page: 1310
  article-title: MicroRNA-22 suppresses DNA repair and promotes genomic instability through targeting of MDC1
  publication-title: Cancer Res
– volume: 461
  start-page: 1071
  issue: 7267
  year: 2009
  end-page: 1078
  article-title: The DNA-damage response in human biology and disease
  publication-title: Nature
– volume: 13
  start-page: 622
  issue: 8
  year: 2014
  end-page: 638
  article-title: Therapeutic targeting of microRNAs: current status and future challenges
  publication-title: Nat Rev Drug Discov
– volume: 19
  start-page: 92
  issue: 1
  year: 2008
  end-page: 105
  article-title: Most mammalian mRNAs are conserved targets of microRNAs
  publication-title: Genome Res
– volume: 60
  start-page: 368
  issue: 4
  year: 2017
  end-page: 375
  article-title: Prediction of pathological complete response using endoscopic findings and outcomes of patients who underwent watchful waiting after chemoradiotherapy for rectal cancer
  publication-title: Dis Colon Rectum
– volume: 20
  start-page: 420
  issue: 4
  year: 2019
  end-page: 432
  article-title: Inflammatory macrophage dependence on NAD+ salvage is a consequence of reactive oxygen species–mediated DNA damage
  publication-title: Nat Immunol
– volume: 6
  start-page: 235
  issue: 3
  year: 2016
  end-page: 246
  article-title: miRNA deregulation in cancer cells and the tumor microenvironment
  publication-title: Cancer Discov
– volume: 8
  start-page: 1442
  issue: 7
  year: 2016
  end-page: 1456
  article-title: miR-638 suppresses DNA damage repair by targeting SMC1A expression in terminally differentiated cells
  publication-title: Aging (Albany NY)
– volume: 4
  start-page: 712
  issue: 9
  year: 2003
  end-page: 720
  article-title: Mechanism and regulation of human non-homologous DNA end-joining
  publication-title: Nat Rev Mol Cell Bio
– volume: 149
  start-page: 515
  issue: 3
  year: 2012
  end-page: 524
  article-title: Roles for microRNAs in conferring robustness to biological processes
  publication-title: Cell
– volume: 36
  start-page: 478
  issue: 9
  year: 2011
  end-page: 484
  article-title: miRNA response to DNA damage
  publication-title: Trends Biochem Sci
– volume: 4
  start-page: e647
  issue: 5
  year: 2013
  article-title: Valosin-containing protein regulates the proteasome-mediated degradation of DNA-PKcs in glioma cells
  publication-title: Cell Death Dis
– volume: 78
  start-page: 501
  issue: 2
  year: 2018
  end-page: 515
  article-title: miR-139-5p modulates radiotherapy resistance in breast cancer by repressing multiple gene networks of DNA repair and ROS defense
  publication-title: Cancer Res
– volume: 16
  start-page: 203
  issue: 3
  year: 2017
  end-page: 222
  article-title: MicroRNA therapeutics: towards a new era for the management of cancer and other diseases
  publication-title: Nat Rev Drug Discov
– volume: 21
  start-page: e103
  issue: 3
  year: 2012
  end-page: e109
  article-title: How does preoperative radiotherapy affect the rate of sphincter-sparing surgery in rectal cancer?
  publication-title: Surg Oncol
– volume: 5
  start-page: 445
  issue: 5
  year: 2017
  end-page: 459
  article-title: Orchestration of DNA damage checkpoint dynamics across the human cell cycle
  publication-title: Cell Syst
– volume: 14
  start-page: 1667
  issue: 11
  year: 2014
  end-page: 1683
  article-title: Targeting the microRNA-regulating DNA damage/repair pathways in cancer
  publication-title: Expert Opin Biol Ther
– volume: 14
  start-page: 6546
  issue: 20
  year: 2008
  end-page: 6555
  article-title: DNA double-strand break repair of blood lymphocytes and normal tissues analysed in a preclinical mouse model: implications for radiosensitivity testing
  publication-title: Clin Cancer Res
– volume: 66
  start-page: 129
  issue: 1
  year: 2015
  end-page: 143
  article-title: The DNA damage response: implications for tumor responses to radiation and chemotherapy
  publication-title: Annu Rev Med
– volume: 20
  start-page: 5468
  issue: 21
  year: 2014
  end-page: 5482
  article-title: The retinoblastoma tumor suppressor modulates DNA repair and radioresponsiveness
  publication-title: Clin Cancer Res
– volume: 47
  start-page: 2187
  issue: 6
  year: 2018
  end-page: 2198
  article-title: Regulation of memory CD8+ T cell differentiation by microRNAs
  publication-title: Cell Physiol Biochem
– volume: 37
  start-page: 413
  issue: 3
  year: 2018
  end-page: 426
  article-title: OxyS small RNA induces cell cycle arrest to allow DNA damage repair
  publication-title: EMBO J
– volume: 293
  start-page: 10512
  issue: 27
  year: 2018
  end-page: 10523
  article-title: Nonhomologous DNA end-joining for repair of DNA double-strand breaks
  publication-title: J Biol Chem
– volume: 20
  start-page: 2810
  issue: 12
  year: 2017
  end-page: 2819
  article-title: DNA ligase IV guides end-processing choice during nonhomologous end joining
  publication-title: Cell Rep
– volume: 11
  start-page: 644
  issue: 9
  year: 2011
  end-page: 656
  article-title: MicroRNA regulation by RNA-binding proteins and its implications for cancer
  publication-title: Nat Rev Cancer
– volume: 3
  start-page: 1227
  issue: 8-9
  year: 2004
  end-page: 1235
  article-title: An overview of three new disorders associated with genetic instability: LIG4 syndrome, RS-SCID and ATR-seckel syndrome
  publication-title: DNA Repair
– volume: 37-38
  start-page: 77
  year: 2016
  end-page: 95
  article-title: Systemic mechanisms and effects of ionizing radiation: a new ‘old’ paradigm of how the bystanders and distant can become the players
  publication-title: Semin Cancer Biol
– volume: 292
  start-page: 3531
  issue: 8
  year: 2017
  end-page: 3540
  article-title: miR-21-mediated radioresistance occurs via promoting repair of DNA double strand breaks
  publication-title: J Biol Chem
– ident: bibr27-1559325820936906
  doi: 10.1038/nrm1202
– ident: bibr29-1559325820936906
  doi: 10.1126/scitranslmed.aac5671
– ident: bibr33-1559325820936906
  doi: 10.1038/nrd.2016.246
– ident: bibr6-1559325820936906
  doi: 10.1016/j.suronc.2012.03.004
– ident: bibr15-1559325820936906
  doi: 10.1158/0008-5472.CAN-14-2783
– ident: bibr18-1559325820936906
  doi: 10.1158/0008-5472.CAN-16-3105
– ident: bibr17-1559325820936906
  doi: 10.1016/j.cels.2017.09.015
– ident: bibr4-1559325820936906
  doi: 10.1038/cddis.2013.171
– ident: bibr20-1559325820936906
  doi: 10.1016/j.cell.2012.04.005
– ident: bibr28-1559325820936906
  doi: 10.1158/1078-0432.CCR-07-5147
– ident: bibr11-1559325820936906
  doi: 10.1038/nrg3765
– ident: bibr9-1559325820936906
  doi: 10.1038/nrc3107
– ident: bibr14-1559325820936906
  doi: 10.18632/aging.100998
– ident: bibr19-1559325820936906
  doi: 10.1158/1078-0432.CCR-14-0326
– ident: bibr12-1559325820936906
  doi: 10.1159/000491532
– ident: bibr31-1559325820936906
  doi: 10.1517/14712598.2014.950650
– ident: bibr21-1559325820936906
  doi: 10.1158/2159-8290.CD-15-0893
– ident: bibr3-1559325820936906
  doi: 10.1146/annurev-med-081313-121208
– ident: bibr25-1559325820936906
  doi: 10.1016/j.dnarep.2004.03.025
– ident: bibr24-1559325820936906
  doi: 10.1074/jbc.TM117.000374
– ident: bibr16-1559325820936906
  doi: 10.15252/embj.201797651
– ident: bibr22-1559325820936906
  doi: 10.1074/jbc.M116.772392
– ident: bibr1-1559325820936906
  doi: 10.1038/s41590-019-0336-y
– ident: bibr26-1559325820936906
  doi: 10.1038/nature08467
– ident: bibr32-1559325820936906
  doi: 10.1038/nrd4359
– ident: bibr23-1559325820936906
  doi: 10.1038/s41416-018-0192-9
– ident: bibr5-1559325820936906
  doi: 10.1016/j.celrep.2017.08.091
– ident: bibr10-1559325820936906
  doi: 10.1101/gr.082701.108
– ident: bibr8-1559325820936906
  doi: 10.1016/j.tibs.2011.06.002
– ident: bibr13-1559325820936906
  doi: 10.1053/j.gastro.2015.05.057
– ident: bibr2-1559325820936906
  doi: 10.1016/j.semcancer.2016.02.002
– ident: bibr7-1559325820936906
  doi: 10.1097/DCR.0000000000000742
– ident: bibr30-1559325820936906
  doi: 10.1093/nar/gkv273
SSID ssj0045731
Score 2.275302
Snippet DNA is subject to a range of endogenous and exogenous insults that can impair DNA replication and lead to DNA double-strand breaks (DSBs). The repair capacity...
SourceID doaj
pubmedcentral
proquest
crossref
sage
SourceType Open Website
Open Access Repository
Aggregation Database
Enrichment Source
Index Database
Publisher
StartPage 155932582093690
SubjectTerms Cell cycle
Cell growth
Colorectal cancer
Deoxyribonucleic acid
DNA
DNA damage
Noncoding RNA: An Emerging Player for Dose-Response Research
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3di9QwEA9y-CCI-InVUyKI4EPZJm3S5vFuz1PhXGQ54V6kzLQJFtbusd27v_8mSXdv90B98TVJ23zMZH6TTH_D2HvTtkZXVpN-IzkoxjYpGlmmoDLUZFGKHANl_lk5m1UXF-b7TqovHxMW6YHjxE2yAmWZOTQOfUgiyZe2iI621cpUBQZoRKhn40zFPbhQZS5uLyUn_u4tl4qsnc9f57Mb7RihwNW_BzDvhkfuxHgFs3P6mD0a8SI_iv18wu7Z_il7GA_bePyH6Bn7-a2bp0JVJZ_H1PJ24CezI34Cv-mVVHgJ3YpD33KCe3wObbccfOB6zBzBl45P51M-tYvFwK874OchPJyMGj_7-rl4zn6cfjqffknHvAlpQ3hmnULrhDVKgiPvE4QG8kKdbosKijxDkDZrG5RtXmWQaVAGLRowLsfGSY2g8xfsoF_29iXjguBFhrlyjrxXAAEF7UqEOaRqCDmhTthkM5F1M5KK-9wWi1qMPOJ3pz5hH7dPXEZCjb-0PfZrs23nqbBDAQlIPQpI_S8BSdjhZmXrUT-H2jtatLMRGk7Yu201aZa_LoHeLq9CG-Hp1IRIWLknEXsd2q_pu1-Bo5vkT-lKJeyDl53bD_9pqK_-x1BfswfSHweEwKJDdrBeXdk37H5zve6G1dugITfIXA4W
  priority: 102
  providerName: Directory of Open Access Journals
Title MiR-1587 Regulates DNA Damage Repair and the Radiosensitivity of CRC Cells via Targeting LIG4
URI https://journals.sagepub.com/doi/full/10.1177/1559325820936906
https://www.proquest.com/docview/2425011150
https://www.proquest.com/docview/2421463611
https://pubmed.ncbi.nlm.nih.gov/PMC7315685
https://doaj.org/article/04b270fb9fb14107876ebbf1288984ba
Volume 18
WOSCitedRecordID wos000545657000001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVAON
  databaseName: DOAJ Directory of Open Access Journals
  customDbUrl:
  eissn: 1559-3258
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0045731
  issn: 1559-3258
  databaseCode: DOA
  dateStart: 20030101
  isFulltext: true
  titleUrlDefault: https://www.doaj.org/
  providerName: Directory of Open Access Journals
– providerCode: PRVHPJ
  databaseName: ROAD: Directory of Open Access Scholarly Resources
  customDbUrl:
  eissn: 1559-3258
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0045731
  issn: 1559-3258
  databaseCode: M~E
  dateStart: 20050101
  isFulltext: true
  titleUrlDefault: https://road.issn.org
  providerName: ISSN International Centre
– providerCode: PRVPQU
  databaseName: Health & Medical Collection
  customDbUrl:
  eissn: 1559-3258
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0045731
  issn: 1559-3258
  databaseCode: 7X7
  dateStart: 20160101
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/healthcomplete
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: ProQuest Central
  customDbUrl:
  eissn: 1559-3258
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0045731
  issn: 1559-3258
  databaseCode: BENPR
  dateStart: 20160101
  isFulltext: true
  titleUrlDefault: https://www.proquest.com/central
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Publicly Available Content Database
  customDbUrl:
  eissn: 1559-3258
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0045731
  issn: 1559-3258
  databaseCode: PIMPY
  dateStart: 20160101
  isFulltext: true
  titleUrlDefault: http://search.proquest.com/publiccontent
  providerName: ProQuest
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1ba9swFBZruofB2L3MWxc0GIM9mPgm2XoabdpuhTYE00H2MMyRLW2GzM7itL9_R7KSNIX1ZS8GSzKWOToXHR1_HyEfRFUJnimO-i1xgyJU6UsRpT6wQHL0KEksLWT-RTqZZLOZmLqEW-fKKtc20Rrqqi1NjnxkQmPDi86Cz4s_vmGNMqerjkJjj-wbpLJkQPaPTyfTfG2LE5bG4fZwcmTO4OKIodczPHaG5eiWM7KY_TuB5t0yyVu1Xtb9nD3934k_I09c4EmP-pXynDxQzQvyuM_a0f5npJfkx2Wd-yHLUpr3HPWqoyeTI3oCv3FO2LiAekmhqSjGjTSHqm47UwHfU1DQVtNxPqZjNZ939KYGemXrzNE70ovzL8kr8u3s9Gr81XcEDH6JgdHKh0qHSrAING5jIeSA21nNqySDJA4kRCqoShlVcRZAwIEJqaQAoWNZ6ohL4PEBGTRto14TGmKcEsiYaY3bYIAQEjRvGLxErMQQTHKPjNaSKEqHTm5IMuZF6ADJ78rOI582Tyx6ZI57xh4b4W7GGUxt29AufxZORYsgkVEaaCm0NMWvaMm4klKjA89ElkjwyOFawIVT9K7YStcj7zfdqKLm3AUa1V7bMaHBZQtDj6Q7S2pnQrs9Tf3Lgn3jAmY8Yx75aBbf9sX_-tQ398_yLXkUmYyBrT06JIPV8lq9Iw_Lm1XdLYdkL52l9poNnSoNbZYC76bnl9PvfwHO2iH5
linkProvider ProQuest
linkToHtml http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1bb9MwFD4aHRJIiDsiMMBIgMRD1MRJnPgBodEyVq2tqqpI4wEFO7FHpJKUphviT_EbOc6lXSextz3wGjuJL-fqc3w-gFc8TTmLFEP-luigcJXYktPQFoEjGWoU35NVyfxhOB5Hx8d8sgN_2rswJq2ylYmVoE6LxJyRd41pbHDRA-f94qdtUKNMdLWF0KjJ4kj9_oUuW_lu0Mf9fU3pwcdZ79BuUAXsBLX9yhapdhUPqNDomwmXCfTRNEv9SPieIwVVTppImnqRIxwmAi6V5IJrTyaaMimYh9-9Brs-jifqwO5kMJp8aWW_H4SeuwmGdk3Mz8N-1DG4eQZV6ZzyqzACtgzbi2mZ53LLKnV3cOd_W6i7cLsxrMl-zQn3YEfl9-FWfSpJ6stWD-DrKJvabhCFZKpODHCZKkl_vE_64geuAT5ciGxJRJ4StIvJVKRZUZoM_xpigxSa9KY90lPzeUnOMkFmVR49an8yHHzyH8LnK5nhI-jkRa4eA3HRDnOkF2iNbr4QrvBRfKNxRoMETUzJLOi2Ox8nTfV1AwIyj92m4PpFWrHg7fqNRV155JK-HwwxrfuZmuHVg2J5EjciKHZ8SUNHS66lSe5FSc2UlBoNlIhHvhQW7LUEFTeCrIw31GTBy3UziiATVxK5Kk6rPq6pO-e6FoRbJLw1oO2WPPteFTNHhglYFFjwxhD75sf_muqTy0f5Am4czkbDeDgYHz2Fm9ScjlR5VnvQWS1P1TO4npytsnL5vGFdAt-umgn-Avl6fW0
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=MiR-1587+Regulates+DNA+Damage+Repair+and+the+Radiosensitivity+of+CRC+Cells+via+Targeting+LIG4&rft.jtitle=Dose-response&rft.au=Liu%2C+Ruixue&rft.au=Shen%2C+Liping&rft.au=Lin%2C+Chuxian&rft.au=He%2C+Junyan&rft.date=2020-04-01&rft.pub=SAGE+PUBLICATIONS%2C+INC&rft.eissn=1559-3258&rft.volume=18&rft.issue=2&rft_id=info:doi/10.1177%2F1559325820936906
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1559-3258&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1559-3258&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1559-3258&client=summon