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Biomedical subjects

Maria Ferraro

Publications and source records attributed to Maria Ferraro.

4 recordsLinked to original sources
PubMed2006

Role of prostaglandin E2 in the invasiveness, growth and protection of cancer cells in malignant pleuritis.

The recurrence of pleural effusions is a common event in a variety of neoplastic diseases. The objective of this study was to identify the mechanisms promoting the homing and growth of cancer cells within the pleural space. A cancer cell line recovered from malignant pleural fluids (lung adenocarcinoma cell line) that constitutively expresses cyclooxygenase 2 (COX-2) and all types of prostaglandin receptors was studied. It was first demonstrated using a matrigel system, that malignant pleural fluids increase the invasiveness of adenocarcinoma cells more than congestive heart failure (CHF) pleural fluids. Moreover, exposure to exudative malignant, but not to CHF pleural fluids, increased the mRNA (measured by real-time polymerase chain reaction (PCR)) and protein expression of COX-2 (measured by Western blot), as well as the activation and nuclear translocation of nuclear factor kappaB (NFkappaB) in cancer cells. These events are all actively regulated by prostaglandin E2 (PGE2), since the addition of synthetic PGE2 to cancer cells and the depletion of PGE2 from malignant pleural fluids or the inhibition of COX-2 activity significantly increased and reduced these phenomena, respectively. Moreover, malignant pleural effusions and synthetic PGE2 increased the long-term proliferation of cancer cells and reverted the impairment in long-term proliferation due to talc exposure. This study demonstrates that PGE2 present in malignant effusions contributes to cancer expansion and may protect cancer cells by anti-proliferative effects induced by talc.

Adenocarcinoma↗
PubMed2004

Synergistic effects of fluticasone propionate and salmeterol on in vitro T-cell activation and apoptosis in asthma.

BACKGROUND: In asthma T cells are characterized by an increased activation state and by reduced apoptosis. OBJECTIVE: Because the clinical efficacy of inhaled corticosteroids combined with long-acting beta 2 -agonists has been widely demonstrated in asthma, we studied, in vitro, the effect of fluticasone propionate (FP) and salmeterol alone and in combination on the activation and apoptosis of peripheral blood T cells (PBTs), on the expression of phosphorylated nuclear factor kappaB inhibitor (IkappaBalpha), and on the nuclear translocation of glucocorticoid receptor (GR) in PBTs from asthmatic subjects. METHODS: Apoptosis was evaluated on the basis of annexin V binding, whereas the expression of caspases 8 and 3 and phosphorylated IkappaBalpha, as well as the nuclear translocation of the GR, were evaluated by means of Western blot analysis. RESULTS: FP alone increases and salmeterol alone does not affect T-cell apoptosis. The combination of FP and salmeterol significantly increases PBT apoptosis in comparison with FP alone. FP at the lower concentration, when combined with salmeterol, is equivalent to FP at the higher concentration in inducing PBT apoptosis. The synergy in the induction of cell apoptosis is associated with more efficient activation of caspases 8 and 3. FP plus salmeterol is also able to synergistically reduce the expression of phosphorylated IkappaBalpha, thus limiting nuclear factor kappaB activation. The synergy was related to an increased nuclear translocation of the GR. CONCLUSION: This study shows that the combination of FP and salmeterol is able to control PBT activation in asthmatic patients more efficiently than FP alone and with a lower concentration of steroids.

Active Transport, Cell Nucleus↗