Rabbit Anti-Human Cofilin (phospho Ser3) monoclonal antibody, clone H.688.5

Determinations of membrane fatty acid composition and fluidity were used together with acidification activity and viability measurements to characterize the physiological state after freezing of Lactobacillus buchneriR1102 and Bifidobacterium longumR0175 cells harvested in the exponential and stationary growth phases. For both strains, lower membrane fluidity was achieved in cells harvested in the stationary growth phase. This change was linked to a lower unsaturated-to-saturated fatty acid ratio for both strains and a higher cyclic-to-saturated fatty acid ratio for L.buchneriR1102 alone. These membrane properties were linked to survival and to maintenance of acidification activity of the cells after freezing, which differed according to the strain and the growth phase. Survival of B.longumR0175 was increased by 10% in cells with low membrane fluidity and high relative saturated fatty acid contents, without any change in acidification activity. Acidification activity was more degraded (70min) in L.buchneriR1102 cells displaying low membrane fluidity and high saturated and cyclic fatty acid levels. Finally, this study showed that membrane modifications induced by the growth phase differed among bacterial strains in terms of composition. By lowering membrane fluidity, these modifications could be beneficial for survival of B.longumR0175 during the freezing process but detrimental for maintenance of acidification activity of L.buchneriR1102.

MicroRNA-342-3p (miR-342) has been shown to act as a tumor-suppressor in different cancer types. However, the role and therapeutic implications of miR-342 via modulation of Cofilin 1 (CFL1) has not been studied in any type of cancer. Given the importance of Cofilin signalling in breast, this study was undertaken to explore the therapeutic implications of miR-342 and its target CFL1 in breast cancer. Herein, we found that miR-342 was significantly (P < 0.05) downregulated in breast cancer tissues and cell lines. Functional assays revealed that overexpression of miR-342 caused a significant (P < 0.05) inhibition of the proliferation, colony formation, invasion and migration of the MDA-MB-436 and CAMA-1 breast cancer cells via induction of apoptosis. Bioinformatic approaches and the dual luciferase reporter assay confirmed the interaction between miR-342 and its target CFL1. Moreover, we found that CFL1 was aberrantly overexpressed in breast cancer tissues and cell lines. Overexpression of miR-342 caused remarkable depletion in the expression of CFL1 in MDA-MB-436 breast cancer cells. Silencing of CFL1 in CAMA-1 and MDA-MB-436 cells caused remarkable decrease in the proliferation, colony formation and migration of these cells, similar to that of miR-342 ovexpression. However, overexpression of CFL1 in MDA-MB-346 cells could avoid the tumor suppressive effects of miR-342. Our data provide novel information about the implications of miR-342 and its target CFL1 in breast cancer treatment.