C1632 suppresses the migration and proliferation of non-small-cell lung cancer cells involving LIN28 and FGFR1 pathway.

Chemoresistance and migration represent major obstacles in the therapy of non-small-cell lung cancer (NSCLC), which accounts for approximately 85% of lung cancer patients in clinic. In the present study, we report that the compound C1632 is preferentially distributed in the lung after oral administration in vivo with high bioavailability and limited inhibitory effects on CYP450 isoenzymes. We found that C1632 could simultaneously inhibit the expression of LIN28 and block FGFR1 signalling transduction in NSCLC A549 and A549R cells, resulting in significant decreases in the phosphorylation of focal adhesion kinase and the expression of matrix metalloproteinase-9.

Sterols from the Green Alga Ulva australis.

Three new sterols, (24)-5,28-stigmastadiene-3β,24-diol-7-one (), (24)-5,28-stigmastadiene-3β,24-diol-7-one (), and 24 and 24-vinylcholesta-3β,5α,6β,24-tetraol (), together with three known sterols (-) were isolated from the green alga . The structures of the new compounds (-) were elucidated through 1D and 2D nuclear magnetic resonance spectroscopy as well as mass spectrometry. Compounds - were identified as isofucoterol (), 24,28 and 24,28-epoxy-24-ethylcholesterol (), and (24)-stigmastadiene-3β,24-diol () on the basis of spectroscopic data analyses and comparison with those reported in the literature.