Anti-CA9 polyclonal antibody

Land degradation in an abandoned field, such as the loss of palatable species for livestock and low species richness, is a serious problem in Mongolia where the dominant land use is livestock grazing historically. Here, we show the factors limiting vegetation recovery processes after cessation of cropping in a semiarid grassland. We selected fields abandoned in 1990 (CA18), 1999 (CA9), and 2006 (CA2) and continuously grazed grassland (CGG) as a control site. Plant species cover and soil were sampled during summer (June-July) 2008. Soil physicochemical properties were analyzed. Low similarity index of an early succession stage, CA2, with CGG was associated with abundant P and coarse sand. The proportion of coarse sand was not abundant in middle stage (CA9) because of domination by perennial rhizomatous species. In the later stage (CA18), the fine sand proportion did not increase; however, the dominant species were associated with fine sand in CGG. The results suggest the limiting factors of recovery processes in abandoned Mongolian cropland are abundantly available P and coarse sand at an early succession stage (CA2). The small proportion of fine sand in CA18 indicated that the impacts of cropping in Mongolia persist for a long time. Published by Elsevier Ltd.

Hypoxia has been long-time acknowledged as major cancer-promoting microenvironment. In such an energy-restrictive condition, post-transcriptional mechanisms gain importance over the energy-expensive gene transcription machinery. Here we show that the onset of hypoxia-induced cancer stem cell features requires the beta-catenin-dependent post-transcriptional up-regulation of CA9 and SNAI2 gene expression. In response to hypoxia, beta-catenin moves from the plasma membrane to the cytoplasm where it binds and stabilizes SNAI2 and CA9 mRNAs, in cooperation with the mRNA stabilizing protein HuR. We also provide evidence that the post-transcriptional activity of cytoplasmic beta-catenin operates under normoxia in basal-like/triple-negative breast cancer cells, where the beta-catenin knockdown suppresses the stem cell phenotype in vitro and tumor growth in vivo. In such cells, we unravel the generalized involvement of the beta-catenin-driven machinery in the stabilization of EGF-induced mRNAs, including the cancer stem cell regulator IL6. Our study highlights the crucial role of post-transcriptional mechanisms in the maintenance/acquisition of cancer stem cell features and suggests that the hindrance of cytoplasmic beta-catenin function may represent an unprecedented strategy for targeting breast cancer stem/basal-like cells.