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Nitric Oxide. 2019 Dec 1;93:34-43. doi: 10.1016/j.niox.2019.09.008. Epub 2019 Sep 19.

Inhibition of breast tumor growth by N(G)-nitro-l-arginine methyl ester (l-NAME) is accompanied by activation of fibroblasts.

Author information

1
Research Area, Instituto de Oncología Ángel H. Roffo, Universidad de Buenos Aires, Buenos Aires, Argentina.
2
Department of Pathology, Instituto de Oncología Ángel H. Roffo, Universidad de Buenos Aires, Buenos Aires, Argentina.
3
Research Area, Instituto de Oncología Ángel H. Roffo, Universidad de Buenos Aires, Buenos Aires, Argentina; Member of Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina. Electronic address: clodillinsky@institutoroffo.uba.ar.
4
Research Area, Instituto de Oncología Ángel H. Roffo, Universidad de Buenos Aires, Buenos Aires, Argentina; Member of Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina. Electronic address: anamariaeijan@gmail.com.

Abstract

Nitric Oxide (NO) is involved in many physiological and pathological processes. It is generated by a family of NO synthases (NOS), being the inducible isoform, iNOS, responsible for higher amounts of NO. Here, we report that pharmacological inhibition of NO production by l-NAME reduces both viability and MAPK activated signalling pathways in iNOS positive human and murine cancer cell lines. In vivo, using syngeneic models, in parallel with tumor reduction induced by l-NAME, collagen deposition and α-SMA positive stromal cells are observed. This observation takes place only when tumor cells express iNOS. In vitro, l-NAME induces viability and differentiation on fibroblast. Our results reveal that NO inhibition contributes to stimulate proliferation and activation of fibroblasts in parallel with tumor reduction of iNOS positive breast cancer.

KEYWORDS:

Breast cancer; Fibroblast; Nitric oxide; iNOS

PMID:
31542422
DOI:
10.1016/j.niox.2019.09.008

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