Palmitoylethanolamide Reduces Colon Cancer Cell Proliferation and Migration, Influences Tumor Cell Cycle and Exerts In Vivo Chemopreventive Effects.
acylethanolamides
colon cancer
endocannabinoid system
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
16 Apr 2021
16 Apr 2021
Historique:
received:
29
03
2021
revised:
09
04
2021
accepted:
12
04
2021
entrez:
30
4
2021
pubmed:
1
5
2021
medline:
1
5
2021
Statut:
epublish
Résumé
Palmitoylethanolamide (PEA) is an endogenous fatty acid amide related to the endocannabinoid anandamide. PEA exerts intestinal anti-inflammatory effects, but knowledge of its role in colon carcinogenesis is still largely fragmentary. We deepened this aspect by studying the effects of PEA (ultramicronized PEA, um-PEA) on colon cancer cell proliferation, migration and cell cycle as well as its effects in a murine model of colon cancer. Results showed that um-PEA inhibited tumor cell proliferation via peroxisome proliferator-activated receptor α and G protein-coupled receptor 55, induced cell cycle arrest in the G2/M phase, possibly through cyclin B1/CDK1 upregulation, and induced DNA fragmentation. Furthermore, um-PEA reduced tumor cell migration by reducing MMP2 and TIMP1 expression. In vivo administration of um-PEA exerted beneficial effects in the azoxymethane model of colonic tumors, by reducing the number of preneoplastic lesions and tumors. Collectively, our findings provide novel proofs on the effects of um-PEA in colon carcinogenesis.
Identifiants
pubmed: 33923494
pii: cancers13081923
doi: 10.3390/cancers13081923
pmc: PMC8073478
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Università degli Studi di Napoli Federico II
ID : Ricerca di Ateneo
Organisme : Regione Campania
ID : B61G18000470007
Organisme : Ministero dell'Istruzione, dell'Università e della Ricerca
ID : 2017XC73BW
Organisme : Ministero dell'Istruzione, dell'Università e della Ricerca
ID : 2017E84AA4
Références
Br J Pharmacol. 2017 Jun;174(11):1349-1365
pubmed: 27539936
Oncogene. 2020 Feb;39(9):2024-2026
pubmed: 31745295
Ann Oncol. 2018 Apr 1;29(4):1016-1022
pubmed: 29562308
Br J Pharmacol. 2014 Sep;171(17):4026-37
pubmed: 24818658
J Exp Clin Cancer Res. 2016 Sep 20;35(1):148
pubmed: 27644693
FEBS J. 2011 Jan;278(1):16-27
pubmed: 21087457
Gastroenterology. 2010 Jun;138(6):2101-2114.e5
pubmed: 20420949
Fundam Clin Pharmacol. 2002 Aug;16(4):297-302
pubmed: 12570018
BMC Cancer. 2012 Mar 19;12:92
pubmed: 22429826
CA Cancer J Clin. 2020 May;70(3):145-164
pubmed: 32133645
Clin Sci (Lond). 2017 Oct 25;131(21):2611-2626
pubmed: 28954820
J Mol Med (Berl). 2008 Jan;86(1):89-98
pubmed: 17823781
Cell Biosci. 2020 Mar 10;10:31
pubmed: 32175074
Phytother Res. 2016 Jun;30(6):963-70
pubmed: 26929026
PLoS One. 2011;6(10):e26823
pubmed: 22046372
Br J Pharmacol. 2019 Dec;176 Suppl 1:S297-S396
pubmed: 31710714
Int J Mol Sci. 2020 Oct 26;21(21):
pubmed: 33114698
Br J Pharmacol. 2018 Apr;175(7):987-993
pubmed: 29520785
CA Cancer J Clin. 2020 Jan;70(1):7-30
pubmed: 31912902
J Neurochem. 2001 Jan;76(2):594-601
pubmed: 11208922
Br J Pharmacol. 2001 Nov;134(5):945-50
pubmed: 11682441
Pharmacol Res. 2017 May;119:227-236
pubmed: 28193521
Oncogene. 2001 Apr 5;20(15):1803-15
pubmed: 11313928
Nat Protoc. 2007;2(8):1998-2004
pubmed: 17703211
Br J Pharmacol. 2015 Jan;172(1):142-58
pubmed: 25205418
Gut. 2014 Aug;63(8):1300-12
pubmed: 24082036
Naunyn Schmiedebergs Arch Pharmacol. 2001 Jul;364(1):66-73
pubmed: 11485041
Nat Med. 2012 Aug;18(8):1232-8
pubmed: 22820645
Br J Pharmacol. 2018 Jul;175(13):2566-2580
pubmed: 29663308
Nat Clin Pract Gastroenterol Hepatol. 2006 Dec;3(12):670-9
pubmed: 17130877
Trends Biochem Sci. 2005 Nov;30(11):630-41
pubmed: 16236519
FEBS Lett. 2006 Nov 13;580(26):6076-82
pubmed: 17055492