Role of non-neuronal cholinergic system in breast cancer progression.
Life Sci
; 80(24-25): 2281-5, 2007 May 30.
Article
en En
| MEDLINE
| ID: mdl-17276463
ABSTRACT
We have previously reported the expression of functional muscarinic acetylcholine receptors (mAChR) in two different murine mammary adenocarcinoma cell lines LM2 and LM3. Activation of mAChR with carbachol (CARB) increased proliferation in both tumor cell lines in a concentration-dependent manner. In LM3 cells CARB promoted proliferation via M(3) receptor activation by inositol 1,4,5-triphosphate and nitric oxide (NO) production. CARB-induced LM2 cells proliferation needed both M(2) and M(1) receptor activation increasing prostaglandin E(2) liberation and arginase catabolism respectively. Our present results indicate that CARB stimulates LM2 and LM3-induced angiogenesis and tumor growth. This activation follows different patterns. In LM2 tumor, M(1) and M(2) receptors activation stimulates neovascularization by arginase II and cyclooxygenase-2 (COX-2)-derived products while M(1) and M(3) receptors mediate CARB-induced tumor growth by the same effector enzymes. In LM3 tumor, we observe that M(1) and M(2) receptors are involved in agonist-stimulated angiogenesis by COX and NOS1-derived products while tumor growth is stimulated by M(3) and M(2) receptors activation and COX-2-derived prostanoids. Taken together these data present, at least in part, a picture of the regulation that different mAChR subtypes activation exerts on angiogenesis and growth of two different murine mammary adenocarcinomas.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Receptor Muscarínico M1
/
Receptor Muscarínico M2
/
Neoplasias Mamarias Experimentales
Límite:
Animals
Idioma:
En
Revista:
Life Sci
Año:
2007
Tipo del documento:
Article
País de afiliación:
Argentina