Silencing of miR-182 is associated with modulation of tumorigenesis through apoptosis induction in an experimental model of colorectal cancer.
Animals
Apoptosis
/ genetics
Caco-2 Cells
Carcinogenesis
/ genetics
Cell Cycle
/ genetics
Colorectal Neoplasms
/ genetics
Disease Models, Animal
Gene Expression Regulation, Neoplastic
Gene Silencing
HT29 Cells
Heterografts
Humans
Mice
Mice, Inbred NOD
Mice, SCID
MicroRNAs
/ genetics
Transfection
Tumor Burden
/ genetics
Up-Regulation
/ genetics
Apoptosis
Cell proliferation
Colorectal cancer
Tumorigenesis
microRNA
Journal
BMC cancer
ISSN: 1471-2407
Titre abrégé: BMC Cancer
Pays: England
ID NLM: 100967800
Informations de publication
Date de publication:
20 Aug 2019
20 Aug 2019
Historique:
received:
29
05
2019
accepted:
26
07
2019
entrez:
21
8
2019
pubmed:
21
8
2019
medline:
26
2
2020
Statut:
epublish
Résumé
miR-182-5p (miR-182) is an oncogenic microRNA (miRNA) found in different tumor types and one of the most up-regulated miRNA in colorectal cancer (CRC). Although this microRNA is expressed in the early steps of tumor development, its role in driving tumorigenesis is unclear. The effects of miR-182 silencing on transcriptomic profile were investigated using two CRC cell lines characterized by different in vivo biological behavior, the MICOL-14 Endogenous miR-182 expression was higher in MICOL-14 Altogether, these data indicate that increased miR-182 expression may promote cell proliferation, suppress the apoptotic pathway and ultimately confer aggressive traits on CRC cells.
Sections du résumé
BACKGROUND
BACKGROUND
miR-182-5p (miR-182) is an oncogenic microRNA (miRNA) found in different tumor types and one of the most up-regulated miRNA in colorectal cancer (CRC). Although this microRNA is expressed in the early steps of tumor development, its role in driving tumorigenesis is unclear.
METHODS
METHODS
The effects of miR-182 silencing on transcriptomic profile were investigated using two CRC cell lines characterized by different in vivo biological behavior, the MICOL-14
RESULTS
RESULTS
Endogenous miR-182 expression was higher in MICOL-14
CONCLUSIONS
CONCLUSIONS
Altogether, these data indicate that increased miR-182 expression may promote cell proliferation, suppress the apoptotic pathway and ultimately confer aggressive traits on CRC cells.
Identifiants
pubmed: 31429725
doi: 10.1186/s12885-019-5982-9
pii: 10.1186/s12885-019-5982-9
pmc: PMC6700772
doi:
Substances chimiques
MicroRNAs
0
Mirn182 microRNA, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
821Subventions
Organisme : AIRC (IT)
ID : IG 2013 n. 14256
Organisme : Università degli Studi di Padova
ID : PRAT CPDA129789
Organisme : Istituto Oncologico Veneto
ID : 5x1000 Intramural Research Grant 2015
Références
Bioinformatics. 2004 Feb 12;20(3):307-15
pubmed: 14960456
Cancer Res. 2005 Mar 15;65(6):2321-9
pubmed: 15781646
Nat Protoc. 2009;4(1):44-57
pubmed: 19131956
Cancer Res. 2009 Feb 15;69(4):1314-23
pubmed: 19208840
Mol Cell. 2009 Aug 14;35(3):384-93
pubmed: 19683501
J Gastroenterol Hepatol. 2010 Oct;25(10):1674-80
pubmed: 20880178
Clin Exp Metastasis. 2011 Jan;28(1):27-38
pubmed: 21069438
Cell Signal. 2011 Jul;23(7):1076-81
pubmed: 21144894
Int J Oncol. 2011 Aug;39(2):311-8
pubmed: 21573504
J Pathol. 2011 Aug;224(4):448-60
pubmed: 21598247
Gut. 2012 Oct;61(10):1447-53
pubmed: 22052060
J Int Med Res. 2011;39(6):2288-95
pubmed: 22289545
Neoplasia. 2012 Sep;14(9):868-79
pubmed: 23019418
RNA. 2013 Feb;19(2):230-42
pubmed: 23249749
Cell Death Dis. 2013 Jun 06;4:e659
pubmed: 23744359
BMC Genomics. 2013 Aug 29;14:589
pubmed: 23987127
Adv Exp Med Biol. 2013;793:1-19
pubmed: 24104470
Med Oncol. 2014 Jan;31(1):799
pubmed: 24310813
Cancer Res. 2014 Apr 1;74(7):2106-18
pubmed: 24525742
BMC Cancer. 2014 Feb 20;14:109
pubmed: 24555885
Clin Chem Lab Med. 2014 Aug;52(8):1217-27
pubmed: 24615484
J Transl Med. 2014 May 01;12:109
pubmed: 24884732
Oncotarget. 2014 Aug 30;5(16):6611-9
pubmed: 25115394
Nucleic Acids Res. 2015 Apr 20;43(7):e47
pubmed: 25605792
Cancer Biol Ther. 2015;16(2):268-75
pubmed: 25629978
J Natl Cancer Inst. 2015 Feb 06;107(3):null
pubmed: 25663689
Oncol Rep. 2015 May;33(5):2592-8
pubmed: 25738520
BMC Cancer. 2015 Apr 30;15:329
pubmed: 25924769
Br J Cancer. 2015 Jun 30;113(1):83-90
pubmed: 26035698
Sci Rep. 2015 Aug 07;5:12921
pubmed: 26250939
Elife. 2015 Aug 12;4:null
pubmed: 26267216
Thorac Cancer. 2015 Jan;6(1):2-9
pubmed: 26273328
World J Gastroenterol. 2015 Nov 7;21(41):11709-39
pubmed: 26556998
Nucleic Acids Res. 2016 Jan 4;44(D1):D239-47
pubmed: 26590260
Oncotarget. 2016 Jul 5;7(27):42805-42825
pubmed: 27081087
Oncotarget. 2016 Sep 13;7(37):60193-60205
pubmed: 27517623
Br J Cancer. 2017 Mar 14;116(6):762-774
pubmed: 28152545
Mol Carcinog. 2017 Dec;56(12):2669-2680
pubmed: 28767179
Dig Dis Sci. 2017 Dec;62(12):3447-3459
pubmed: 29030743
Sci Rep. 2017 Nov 28;7(1):16495
pubmed: 29184082
Mol Cancer. 2018 Jan 31;17(1):17
pubmed: 29386021