Adaptive Evolution of Defense Ability Leads to Diversification of Prey Species

In this paper, by using the adaptive dynamics approach, we investigate how the adaptive evolution of defense ability promotes the diversity of prey species in an initial one-prey–two-predator community. We assume that the prey species can evolve to a safer strategy such that it can reduce the predation risk, but a prey with a high defense ability for one predator may have a low defense ability for the other and vice versa. First, by using the method of critical function analysis, we find that if the trade-off is convex in the vicinity of the evolutionarily singular strategy, then this singular strategy is a continuously stable strategy. However, if the trade-off is weakly concave near the singular strategy and the competition between the two predators is relatively weak, then the singular strategy may be an evolutionary branching point. Second, we find that after the branching has occurred in the prey strategy, if the trade-off curve is globally concave, then the prey species might eventually evolve into two specialists, each caught by only one predator species. However, if the trade-off curve is convex–concave–convex, the prey species might eventually branch into two partial specialists, each being caught by both of the two predators and they can stably coexist on the much longer evolutionary timescale.     

MiR-489 regulates chemoresistance in breast cancer via epithelial mesenchymal transition pathway

To investigate the role of microRNAs in the development of chemoresistance and related epithelial–mesenchymal transition (EMT), we examined the effect of miR-489 in adriamycin (ADM)-resistant human breast cancer cells (MCF-7/ADM). MiR-489 was significantly suppressed in MCF-7/ADM cells compared with chemosensitive parental control MCF-7/WT cells. Forced-expression of miR-489 reversed chemoresistance. Furthermore, Smad3 was identified as the target of miR-489 and is highly expressed in MCF-7/ADM cells. Forced expression of miR-489 both inhibited Smad3 expression and Smad3 related EMT properties. Finally, the interactions between Smad3, miR-489 and EMT were confirmed in chemoresistant tumor xenografts and clinical samples, indicating their potential implication for treatment of chemoresistance.     

Fish community assemblages changed but biomass remained similar after lake restoration by biomanipulation in a Chinese tropical eutrophic lake

While the effects of lake restoration by fish manipulation are well-studied in the temperate zone, comparatively little information is available on this issue from tropical lakes. It may be expected that fish removal leads to faster recovery of the fish stock here than in temperate lakes due to more frequent and earlier reproduction, which may, in turn, delay positive effects of the restoration. We studied the community composition, feeding type and abundance of fish in three basins of a tropical shallow lake: one unrestored basin (UR) and two basins restored by fish manipulation and transplantation of submerged macrophytes. While omni-benthivorous fish dominated the biomass in the restored basins 3 and 5 years after restoration, planktivores were most abundant in the UR, although total fish biomass remained similar. One-way analyses of similarities based on fish species presence/absence, abundance and biomass data revealed significant differences in fish community composition among the restored basins and UR, and redundancy analyses further indicated that submerged macrophytes were a key driver behind this difference. Our results indicate that active implantation of submerged macrophytes to stabilise the fish community is a tool to consider when planning lake restoration by biomanipulation in the tropics.     

Anti-osteopontin monoclonal antibody prevents ovariectomy-induced osteoporosis in mice by promotion of osteoclast apoptosis

Osteopontin (OPN) is abundant in mineralized tissues and has long been implicated in bone remodeling. However, the therapeutic effect of targeting OPN in bone loss diseases and the underlying molecular mechanism remain largely unknown. Here, we reported that anti-OPN mAb (23C3) could protect against ovariectomy-induced osteoporosis in mice, demonstrated by microcomputed tomography analysis and histopathology evaluation. In vitro assay showed that 23C3 mAb reduced osteoclasts (OCs)-mediated bone resorption through promotion of mature OC apoptosis. Thus, the study has important implications for understanding the role of OPN in OC bone resorption and survival, and OPN antagonists may have therapeutic potential for osteoporosis and other osteopenic diseases.     

MicroRNA-145 suppresses hepatocellular carcinoma by targeting IRS1 and its downstream Akt signaling

Accumulating evidences have proved that dysregulation of microRNAs (miRNAs) is involved in cancer initiation and progression. In this study, we showed that miRNA-145 level was significantly decreased in hepatocellular cancer (HCC) tissues and cell lines, and its low expression was inversely associated with the abundance of insulin receptor substrate 1 (IRS1), a key mediator in oncogenic insulin-like growth factor (IGF) signaling. We verified IRS1 as a direct target of miR-145 using Western blotting and luciferase reporter assay. Further, the restoration of miR-145 in HCC cell lines suppressed cancer cell growth, owing to down-regulated IRS1 expression and its downstream Akt/FOXO1 signaling. Our results demonstrated that miR-145 could inhibit HCC through targeting IRS1 and its downstream signaling, implicating the loss of miR-145 regulation may be a potential molecular mechanism causing aberrant oncogenic signaling in HCC.     

HepG2.2.15 as a model for studying cell protrusion and migration regulated by S100 proteins

Much of the difficulty in elucidating the precise function of S100 protein family has been attributed to functional redundancy and compensation by its conserved family members. In this study, we showed that seven S100 family members were almost totally undetectable in HepG2.2.15 cells, while all of them were highly expressed in its parental HepG2 cells. Re-expression of S100 proteins in HepG2.2.15 cells can partially rescue their defects in cell protrusion and migration through the regulation of cytoskeletons and adhesions. Thus, HepG2.2.15 can serve as a useful model for studying cell protrusion and migration regulated by S100 proteins.