Anticancer activity of emodin is associated with downregulation of CD155.
Animals
Antineoplastic Agents
/ pharmacology
Cell Line, Tumor
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Down-Regulation
Emodin
/ pharmacology
Female
Melanoma, Experimental
/ drug therapy
Mice, Inbred C57BL
RNA, Small Interfering
/ genetics
Receptors, Virus
/ genetics
Skin Neoplasms
/ drug therapy
Tumor Burden
/ drug effects
Adhesion molecule
CD155
Emodin
Herb-derived compound
Tumor
Journal
International immunopharmacology
ISSN: 1878-1705
Titre abrégé: Int Immunopharmacol
Pays: Netherlands
ID NLM: 100965259
Informations de publication
Date de publication:
Oct 2019
Oct 2019
Historique:
received:
18
03
2019
revised:
13
07
2019
accepted:
13
07
2019
pubmed:
22
7
2019
medline:
15
2
2020
entrez:
21
7
2019
Statut:
ppublish
Résumé
Emodin is a Chinese herb-derived compound that exhibits a variety of pharmacological benefits. Although emodin has been shown to inhibit growth of cancer cells, its antineoplastic function is incompletely understood. CD155 is a member of poliovirus receptor-related (PRR) family of adhesion molecules; it is constitutively expressed on many tumor cell lines and tissues and has diverse functions. CD155 has been reported to mediate activation of T cells via CD226 or inhibition of T cells via T-cell immunoreceptor with Ig and ITIM domains (TIGIT). In addition, CD155 may play a critical role through non-immunological mechanisms in cancer. In this study, we tested the ability of emodin to modulate CD155 expression in cancer cells. We found that emodin significantly decreased the expression of CD155 in tumor cells and inhibited tumor cell proliferation and migration, and induced cell-cycle arrest at G2/M phase. The tumor inhibitory effects of emodin were lost with CD155 knockdown. Furthermore, emodin was used to treat mice bearing B16 melanoma. It was shown that emodin attenuated tumor growth accompanied by suppressing CD155 expression. Therefore, we propose that emodin could inhibit tumor growth, and the antineoplastic properties of emodin are at least partially CD155 dependent. Our study provides new insights into the mechanisms by which emodin inhibits tumor growth.
Identifiants
pubmed: 31325728
pii: S1567-5769(19)30570-3
doi: 10.1016/j.intimp.2019.105763
pmc: PMC7020937
mid: NIHMS1535053
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
RNA, Small Interfering
0
Receptors, Virus
0
poliovirus receptor
0
Emodin
KA46RNI6HN
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
105763Subventions
Organisme : NCI NIH HHS
ID : R01 CA218578
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL116626
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA216230
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.
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