Lack of effect of the procarcinogenic 17 beta-estradiol on nutrient uptake by the MCF-7 breast cancer cell line

• Tipo: Artigo em Revista Científica Internacional
• Data: 2017

Autores

Nunes, C (Autor) Outra; Silva, C (Autor) Outra; Correia Branco, A (Autor) Outra; Martel, F (Autor) FMUP

Revista

Título: Biomedicine & Pharmacotherapy

Vol. 90

Páginas: 287-294

ISSN: 0753-3322

Editora: Elsevier

Indexação

ISI Web of Knowledge - 4 Citações

Scopus - 5 Citações

Outras Informações

ID Authenticus: P-00M-KMX

DOI: 10.1016/j.biopha.2017.03.069

Abstract (EN): Breast cancer is one of the most frequent cancers in the population, especially in older women. Estrogen is known to be a key hormone in the development and progression of mammary carcinogenesis. In this study, we investigated if the procarcinogenic effect of 17 beta-estradiol (E2) in breast cancer MCF-7 cells is dependent on changes in glucose or folic acid cellular uptake. The effect of E2 on uptake of H-3-deoxy-D-glucose, H-3-folic acid, cell proliferation (3-thymidine incorporation assay), culture growth (sulforhodamine B assay), viability (lactate dehydrogenase activity assay), lactate production and migration capacity (injury assay) was evaluated. E2 (48 h; 100 nM) increased culture growth (16%), proliferation rate (24%), cellular viability (36%) and lactate production (38%). In contrast, E2 did not significantly affect the migration capacity of MCF-7 cells. The pro-proliferative, but not the cytoprotective effect of E2 was found to be ERb-dependent. The polyphenols rutin and caffeic acid were not able to counteract the effect of E2 upon cell proliferation and viability. Uptake of H-3-deoxy-D-glucose was not affected by E2, either in the absence or presence of GLUT inhibitors (cytochalasin B plus phloridzin). Moreover, E2 did not change GLUT1 mRNA levels. Finally, H-3-folic acid uptake was also not affected by E2, both in the absence and presence of the RFC1 inhibitor, methotrexate. The pro-proliferative and cytoprotective effects of E2 are not dependent neither of stimulation of glucose cellular uptake (both GLUT and non-GLUT-mediated) nor of stimulation of folic acid uptake (both RFC1- and non-RFC1-mediated).

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 8