Nicotine Synergizes with High-Fat Diet to Induce an Anti-Inflammatory Microenvironment to Promote Breast Tumor Growth.
Animal Feed
Animals
Anti-Inflammatory Agents
/ pharmacology
Breast Neoplasms
/ chemically induced
Cell Line, Tumor
Cell Proliferation
Diet, High-Fat
Female
Humans
Imidazoles
/ pharmacology
Inflammasomes
Inflammation
Mammary Neoplasms, Animal
/ chemically induced
Mecamylamine
/ chemistry
Mice
Neoplasm Transplantation
Neoplastic Stem Cells
/ metabolism
Nicotine
/ chemistry
Oxidative Stress
/ drug effects
Pyridines
/ pharmacology
Up-Regulation
p38 Mitogen-Activated Protein Kinases
/ metabolism
Journal
Mediators of inflammation
ISSN: 1466-1861
Titre abrégé: Mediators Inflamm
Pays: United States
ID NLM: 9209001
Informations de publication
Date de publication:
2020
2020
Historique:
received:
09
07
2020
revised:
26
10
2020
accepted:
25
11
2020
entrez:
8
1
2021
pubmed:
9
1
2021
medline:
22
9
2021
Statut:
epublish
Résumé
Breast cancer results from a complex interplay of genetics and environment that alters immune and inflammatory systems to promote tumorigenesis. Obesity and cigarette smoking are well-known risk factors associated breast cancer development. Nicotine known to decrease inflammatory signals also modulates immune responses that favor breast cancer development. However, the mechanisms by which nicotine and obesity contribute to breast cancer remain poorly understood. In this study, we examined potential mechanisms by which nicotine (NIC) and high-fat diet (HFD) promote growth of HCC70 and HCC1806 xenografts from African American (AA) triple negative (TN) breast cancer cells. Immunodeficient mice fed on HFD and treated with NIC generated larger HCC70 and HCC1806 tumors when compared to NIC or HFD alone. Increased xenograft growth in the presence of NIC and HFD was accompanied by higher levels of tissue-resident macrophage markers and anti-inflammatory cytokines including IL4, IL13, and IL10. We further validated the involvement of these players by
Identifiants
pubmed: 33414685
doi: 10.1155/2020/5239419
pmc: PMC7752272
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Imidazoles
0
Inflammasomes
0
Pyridines
0
Mecamylamine
6EE945D3OK
Nicotine
6M3C89ZY6R
p38 Mitogen-Activated Protein Kinases
EC 2.7.11.24
SB 203580
OU13V1EYWQ
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5239419Subventions
Organisme : NCI NIH HHS
ID : SC1 CA165865
Pays : United States
Organisme : NIMHD NIH HHS
ID : U54 MD007598
Pays : United States
Organisme : NIA NIH HHS
ID : SC1 AG049682
Pays : United States
Organisme : NCI NIH HHS
ID : SC1 CA232319
Pays : United States
Organisme : NIMHD NIH HHS
ID : S21 MD000103
Pays : United States
Informations de copyright
Copyright © 2020 Thalia Jimenez et al.
Déclaration de conflit d'intérêts
The authors declare that they have no conflict of interest.
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