Vibrational analysis of d-PCL(530)/siloxane based hybrids doped with two lithium salts

Published online: 22 May 2013The present study has been focused on environmentally friendly sol-gel derived electrolytes based on a di-urethane cross-linked d-PCL(530)/siloxane network (where d represents di, PCL identifies the poly(ε–caprolactone) biopolymer and 530 is the average molecular weight in g.mol-1) doped with a wide range of concentration of lithium perchlorate (LiClO4) and lithium bis(trifluoromethanesulfonyl)imide (LiTFSI). Fourier Transform Infrared and Raman (FT-IR and FT-Raman, respectively) spectroscopies have been applied to evaluate the extent of ionic association. Characteristic bands of the PCL(530) segments, of the urethane cross-links and of the anions have been examined to gain insight into the cation/biopolymer, cation/anion and cation/cross-link interactions. In both electrolyte systems “free” ions and contact ions have been identified. The addition of salt modifies the hydrogen-bonded array of the host matrix, causing the destruction/formation of the urethane/urethane aggregates.Fundação para a Ciência e a Tecnologia (FCT

GP88 (PC-Cell Derived Growth Factor, progranulin) stimulates proliferation and confers letrozole resistance to aromatase overexpressing breast cancer cells

<p>Abstract</p> <p>Background</p> <p>Aromatase inhibitors (AI) that inhibit breast cancer cell growth by blocking estrogen synthesis have become the treatment of choice for post-menopausal women with estrogen receptor positive (ER⁺) breast cancer. However, some patients display de novo or acquired resistance to AI. Interactions between estrogen and growth factor signaling pathways have been identified in estrogen-responsive cells as one possible reason for acquisition of resistance. Our laboratory has characterized an autocrine growth factor overexpressed in invasive ductal carcinoma named PC-Cell Derived Growth Factor (GP88), also known as progranulin. In the present study, we investigated the role GP88 on the acquisition of resistance to letrozole in ER⁺breast cancer cells</p> <p>Methods</p> <p>We used two aromatase overexpressing human breast cancer cell lines MCF-7-CA cells and AC1 cells and their letrozole resistant counterparts as study models. Effect of stimulating or inhibiting GP88 expression on proliferation, anchorage-independent growth, survival and letrozole responsiveness was examined.</p> <p>Results</p> <p>GP88 induced cell proliferation and conferred letrozole resistance in a time- and dose-dependent fashion. Conversely, naturally letrozole resistant breast cancer cells displayed a 10-fold increase in GP88 expression when compared to letrozole sensitive cells. GP88 overexpression, or exogenous addition blocked the inhibitory effect of letrozole on proliferation, and stimulated survival and soft agar colony formation. In letrozole resistant cells, silencing GP88 by siRNA inhibited cell proliferation and restored their sensitivity to letrozole.</p> <p>Conclusion</p> <p>Our findings provide information on the role of an alternate growth and survival factor on the acquisition of aromatase inhibitor resistance in ER⁺breast cancer.</p