Publications

Abstract: Social environmental conditions, particularly the experience of social adversity, have long been connected with health and mortality in humans and other social mammals. Efforts to identify the physiological basis for these effects have historically focused on their neurological, endocrinological, and immunological consequences. Recently, this search has been extended to understanding the role of gene regulation in sensing, mediating, and determining susceptibility to social environmental variation. Studies in laboratory rodents, captive primates, and human populations have revealed correlations between social conditions and the regulation of a large number of genes, some of which are likely causal. Gene expression responses to the social environment are, in turn, mediated by a set of underlying regulatory mechanisms, of which epigenetic marks are the best studied to date. Importantly, a number of genes involved in the response to the social environment are also associated with susceptibility to other external stressors, as well as certain diseases. Hence, gene regulatory studies are a promising avenue for understanding, and potentially developing strategies to address, the effects of social adversity on health.

Abstract: The abundance of an mRNA in a cell depends on its overall rates of synthesis and decay. RNA stability is an important element in the regulation of gene expression, and is achieved by a variety of processes including specific recruitment of nucleases and RNAi-associated mechanisms. These mechanisms are particularly important in stem cells, which, in many cases, have attenuated transcription. Here we report that mRNA injected into fertilized eggs of the sea urchin is selectively retained in the small micromeres,which contribute to the germline in this organism, beginning in blastulae, when compared to adjacent somatic cells. We show that modification of this exogenous RNA using cap analogs and poly-adenosine tail deletions do not affect its selective retention in the small micromeres, but removal of the cap or of the 3'-untranslated region eliminates any selective mRNA retention in the germline. Our results illuminate a likely ancient mechanism used by stem cells to prolong the lifespan of RNAs – either through RNA protection or by the absence of basic RNA degradation mechanisms, which are employed by most other cells of an organism. Mol. Reprod. Dev. (c) 2013 Wiley Periodicals, Inc.

Abstract: Triple-negative (ER-/PR-/HER2-) breast cancer (TNBC) is a severe clinical problem because of its relatively poorer prognosis, aggressive behaviour and lack of targeted therapies. Naringin, a major flavonoid extracted from citrus fruits, has been reported to exert promising anticancer activities. However, the detailed antitumor mechanism of naringin still remains enigmatic. In this study, TNBC cell lines-based in vitro and in vivo models were used to explore the anticancer effect and mechanism of naringin. Our data demonstrated that naringin inhibited cell proliferation, and promoted cell apoptosis and G1 cycle arrest, accompanied by increased p21 and decreased survivin. Meanwhile, beta-catenin signaling pathway was found to be suppressed by naringin. In contrast, over-expressing beta-catenin by adenoviral vector system in TNBC cells reversed the antitumor activity of naringin, and regulated p21 and survivin. Correspondingly, the antitumor potential of naringin was also observed in naringin-treated MDA-MB-231 xenograft mice, while immunohistochemical analysis of tumors from naringin-treated mice showed higher expression of p21 and lower expression of survivin and active beta-catenin. Taken together, these results indicate that naringin could inhibit growth potential of TNBC cells by modulating beta-catenin pathway, which suggests naringin might be used as a potential supplement for the prevention and treatment of breast cancer.