Effects ofAgeratina adenophoraInvasion on the Understory Community and Soil Phosphorus Characteristics of Different Forest Types in Southwest China

Understanding the influence of invasive species on community composition and ecosystem properties is necessary to maintain ecosystem functions. However, little is known about how understory plant communities and soil nutrients respond to invasion under different land cover types. Here, we investigated the effects of the invasive species Ageratina adenophora on the species and functional diversity of understory communities and on soil phosphorus (P) status in three forest types: CF, coniferous forest; MF, coniferous and broadleaf mixed forest; and EBF, evergreen broadleaf forest. We found that the species and functional diversity indices of the understory community significantly varied by forest type. Among the invaded plots, the greatest decrease in functional diversity (functional richness, functional divergence, and functional dispersion) and biotic homogenization were found in the CF rather than the MF or EBF. In addition, the invasion by A. adenophora significantly increased the soil NaHCO3-extractable inorganic P and organic P in the MF and EBF, respectively, while obviously decreasing the soil maximum P sorption capacity and maximum buffering capacity in the CF. However, the changes in the species and functional attributes of the understory communities were weakly associated with changes in the soil P status, probably because of the different response times to invasion in different forest types. The implication of these changes for ecosystem structure and function must be separately considered when predicting and managing invasion at a landscape scale

Re-expression of ARHI (DIRAS3) induces autophagy in breast cancer cells and enhances the inhibitory effect of paclitaxel

<p>Abstract</p> <p>Background</p> <p><it>ARHI </it>is a Ras-related imprinted gene that inhibits cancer cell growth and motility. ARHI is downregulated in the majority of breast cancers, and loss of its expression is associated with its progression from ductal carcinoma <it>in situ </it>(DCIS) to invasive disease. In ovarian cancer, re-expression of ARHI induces autophagy and leads to autophagic death in cell culture; however, ARHI re-expression enables ovarian cancer cells to remain dormant when they are grown in mice as xenografts. The purpose of this study is to examine whether ARHI induces autophagy in breast cancer cells and to evaluate the effects of ARHI gene re-expression in combination with paclitaxel.</p> <p>Methods</p> <p>Re-expression of ARHI was achieved by transfection, by treatment with trichostatin A (TSA) or by a combination of TSA and 5-aza-2'-deoxycytidine (DAC) in breast cancer cell cultures and by liposomal delivery of ARHI in breast tumor xenografts.</p> <p>Results</p> <p>ARHI re-expression induces autophagy in breast cancer cells, and ARHI is essential for the induction of autophagy. When ARHI was re-expressed in breast cancer cells treated with paclitaxel, the growth inhibitory effect of paclitaxel was enhanced in both the cell culture and the xenografts. Although paclitaxel alone did not induce autophagy in breast cancer cells, it enhanced ARHI-induced autophagy. Conversely, ARHI re-expression promoted paclitaxel-induced apoptosis and G2/M cell cycle arrest.</p> <p>Conclusions</p> <p>ARHI re-expression induces autophagic cell death in breast cancer cells and enhances the inhibitory effects of paclitaxel by promoting autophagy, apoptosis, and G2/M cell cycle arrest.</p