Exosomal miR-224-5p from Colorectal Cancer Cells Promotes Malignant Transformation of Human Normal Colon Epithelial Cells by Promoting Cell Proliferation through Downregulation of CMTM4.
Journal
Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826
Informations de publication
Date de publication:
2022
2022
Historique:
received:
06
12
2021
accepted:
23
05
2022
entrez:
11
7
2022
pubmed:
12
7
2022
medline:
14
7
2022
Statut:
epublish
Résumé
Interactions between malignant cells and neighboring normal cells are important for carcinogenesis. In addition, cancer cell-derived exosomes have been shown to promote the malignant transformation of recipient cells, but the mechanisms remain unclear. The level of miR-224-5p in CRC cell-derived exosomes was determined by RT-qPCR assay. In addition, PKH26 dye-labeled exosomes were used to assess the efficacy of the transfer of exosomes between SW620 and normal colon epithelial cell line CCD 841 CoN. In this study, we found that overexpression of miR-224-5p significantly promoted the proliferation, migration, and invasion and inhibited the oxidative stress of SW620 cells. In addition, miR-224-5p can be transferred from SW620 cells to CCD 841 CoN cells via exosomes. SW620 cell-derived exosomal miR-224-5p markedly promoted proliferation, migration, and invasion of CCD 841 CoN cells. Meanwhile, SW620 cell-derived exosomal miR-224-5p notably decreased the expression of CMTM4 in CCD 841 CoN cells. Furthermore, SW620 cell-derived exosomal miR-224-5p significantly promoted tumor growth in a xenograft model These findings suggested that SW620 cell-derived exosomal miR-224-5p could promote malignant transformation and tumorigenesis
Sections du résumé
Background
UNASSIGNED
Interactions between malignant cells and neighboring normal cells are important for carcinogenesis. In addition, cancer cell-derived exosomes have been shown to promote the malignant transformation of recipient cells, but the mechanisms remain unclear.
Methods
UNASSIGNED
The level of miR-224-5p in CRC cell-derived exosomes was determined by RT-qPCR assay. In addition, PKH26 dye-labeled exosomes were used to assess the efficacy of the transfer of exosomes between SW620 and normal colon epithelial cell line CCD 841 CoN.
Results
UNASSIGNED
In this study, we found that overexpression of miR-224-5p significantly promoted the proliferation, migration, and invasion and inhibited the oxidative stress of SW620 cells. In addition, miR-224-5p can be transferred from SW620 cells to CCD 841 CoN cells via exosomes. SW620 cell-derived exosomal miR-224-5p markedly promoted proliferation, migration, and invasion of CCD 841 CoN cells. Meanwhile, SW620 cell-derived exosomal miR-224-5p notably decreased the expression of CMTM4 in CCD 841 CoN cells. Furthermore, SW620 cell-derived exosomal miR-224-5p significantly promoted tumor growth in a xenograft model
Conclusion
UNASSIGNED
These findings suggested that SW620 cell-derived exosomal miR-224-5p could promote malignant transformation and tumorigenesis
Identifiants
pubmed: 35814269
doi: 10.1155/2022/5983629
pmc: PMC9262543
doi:
Substances chimiques
CMTM4 protein, human
0
MARVEL Domain-Containing Proteins
0
MIRN224 microRNA, human
0
MicroRNAs
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5983629Informations de copyright
Copyright © 2022 Feng Wu et al.
Déclaration de conflit d'intérêts
The authors declare no potential conflicts of interest.
Références
Mol Ther Nucleic Acids. 2019 Dec 6;18:232-244
pubmed: 31563120
Cell Oncol (Dordr). 2021 Feb;44(1):45-59
pubmed: 33423167
Expert Opin Biol Ther. 2012 Jun;12 Suppl 1:S199-207
pubmed: 22509743
Clin Cancer Res. 2017 Sep 1;23(17):5311-5319
pubmed: 28606918
Cancer Biol Ther. 2016 Oct 2;17(10):1062-1069
pubmed: 27611932
World J Gastroenterol. 2018 Jul 21;24(27):2949-2973
pubmed: 30038463
Adv Exp Med Biol. 2007;593:117-33
pubmed: 17265722
Eur Rev Med Pharmacol Sci. 2017 Nov;21(21):5008-5016
pubmed: 29164556
Cancer Sci. 2020 Dec;111(12):4348-4358
pubmed: 32969511
J Exp Clin Cancer Res. 2020 Feb 10;39(1):32
pubmed: 32039741
Oncol Rep. 2016 May;35(5):2499-515
pubmed: 26986034
Br J Cancer. 2020 May;122(11):1630-1637
pubmed: 32238921
Harefuah. 2017 Nov;156(11):710-714
pubmed: 29198089
Oncogene. 2020 Apr;39(14):2863-2876
pubmed: 32034309
Genes Chromosomes Cancer. 2017 Nov;56(11):769-787
pubmed: 28675510
J Exp Clin Cancer Res. 2019 Nov 12;38(1):465
pubmed: 31718693
Biomed Res Int. 2019 Sep 17;2019:9740568
pubmed: 31637261
Nat Rev Immunol. 2015 Nov;15(11):669-82
pubmed: 26471778
J Exp Clin Cancer Res. 2015 Oct 16;34:122
pubmed: 26474560
Dig Liver Dis. 2009 Dec;41(12):875-80
pubmed: 19473897
Nat Commun. 2018 Dec 19;9(1):5395
pubmed: 30568162
Cancer Cell. 2014 Apr 14;25(4):501-15
pubmed: 24735924
Nat Cell Biol. 2018 May;20(5):597-609
pubmed: 29662176
Radiat Oncol. 2012 Jun 09;7:83
pubmed: 22681700
Int J Mol Sci. 2020 Mar 31;21(7):
pubmed: 32244500
Sci Rep. 2017 Jul 19;7(1):5918
pubmed: 28724995
J Nanobiotechnology. 2021 Aug 12;19(1):242
pubmed: 34384440
3 Biotech. 2020 Nov;10(11):485
pubmed: 33117626
J Mol Med (Berl). 2013 Apr;91(4):431-7
pubmed: 23519402
Acta Biochim Biophys Sin (Shanghai). 2019 Sep 6;51(9):915-924
pubmed: 31435638
Oxid Med Cell Longev. 2016;2016:6234043
pubmed: 27057283
Asian J Psychiatr. 2019 Feb;40:76-81
pubmed: 30771755
J Clin Invest. 2016 Apr 1;126(4):1208-15
pubmed: 27035812
Oncol Rep. 2018 Dec;40(6):3171-3188
pubmed: 30542718
Cancer Cell. 2016 Dec 12;30(6):836-848
pubmed: 27960084
Int J Med Sci. 2019 Oct 21;16(12):1573-1582
pubmed: 31839745
Mol Cancer. 2019 Mar 19;18(1):43
pubmed: 30890168
EBioMedicine. 2019 Jul;45:208-219
pubmed: 31221586
Adv Cancer Res. 2018;140:121-154
pubmed: 30060807
Cancer Sci. 2021 May;112(5):1839-1852
pubmed: 33205567
J Cell Biol. 2012 Feb 20;196(4):395-406
pubmed: 22351925
Mol Clin Oncol. 2018 Apr;8(4):523-527
pubmed: 29556386
Mol Cancer. 2020 Jul 27;19(1):117
pubmed: 32713345