Boosting Anti-tumour Immunity Using Adjuvant Apigenin.
Apigenin
anti-tumour immunity
cytotoxic CD8+ T Lymphocytes (CTLs)
natural killer (NK) cells
tumour microenvironment (TME)
Journal
Anti-cancer agents in medicinal chemistry
ISSN: 1875-5992
Titre abrégé: Anticancer Agents Med Chem
Pays: Netherlands
ID NLM: 101265649
Informations de publication
Date de publication:
2023
2023
Historique:
received:
21
01
2022
revised:
01
04
2022
accepted:
06
04
2022
pubmed:
27
5
2022
medline:
10
3
2023
entrez:
26
5
2022
Statut:
ppublish
Résumé
The interactions and secretions within the tumour have a pivotal role in tumour growth and therapy. Immunosuppressive cells such as regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), tumour-associated macrophages (TAMs), and cancer-associated fibroblasts (CAFs) secrete some substances, which can result in the exhaustion of anti-tumour immunity. To stimulate anti-tumour immunity, suppression of the secretion and interactions of immunosuppressive cells, on the other hand, stimulation of proliferation and activation of natural killer (NK) cells and CD8+ T lymphocytes are required. Apigenin is a flavone with anticancer properties. Emerging evidence shows that not only does apigenin modulate cell death pathways in cancer cells but it also can stimulate anti-tumour immune cells to release death signals and suppress the release of tumour-promoting molecules. In this review, we discuss the interactions between apigenin and various cells within the tumour microenvironment (TME). These interactions may enhance anti-tumour immunity to improve the efficiency of anticancer remedies such as immunotherapy.
Identifiants
pubmed: 35616683
pii: ACAMC-EPUB-123874
doi: 10.2174/1871520622666220523151409
doi:
Substances chimiques
Apigenin
7V515PI7F6
Types de publication
Review
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
266-277Informations de copyright
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.