Several outlets report on “Ion channel TRPV1-dependent activation of PTP1B suppresses EGFR-associated intestinal tumorigenesis” by Petrus R. de Jong and colleagues at the University of California at San Diego.
Read how this study suggests that capsaicin may limit intestinal tumorigenesis: Time, New York Daily News, Daily Mail, Business Standard, The Free Press Journal, Science World Report, Deccan Chronicle, Tech Times, Bioscience Technology, and South China Morning Post.
Multiple sources cover "Sexually dimorphic RB inactivation underlies mesenchymal glioblastoma prevalence in males" by Tao Sun and colleagues at Washington University School of Medicine.
This study provides an explanation for why some types of brain tumors are more common in men: Science World Report, International Business Times, Headlines and Global News, Science 2.0, French Tribune, Delhi Daily News, RTT News
Various media sources have stories on "PPARγ ablation sensitizes proopiomelanocortin neurons to leptin during high-fat feeding" by Lihong Long and colleagues at Yale University.
Read more about how proopiomelanocortin-expressing neurons regulate whole-body energy balance: Nature World News, FoxCT, Science 2.0, Headlines and Global News, International Business Times, Tech Times, and Fars News.
The intestinal epithelium has a high rate of turnover, and dysregulation of pathways that regulate regeneration can lead to tumor development; however, the negative regulators of oncogenic events in the intestinal epithelium are not fully understood. Here we identified a feedback loop between the epidermal growth factor receptor (EGFR), a known mediator of proliferation, and the transient receptor potential cation channel, subfamily V, member 1 (TRPV1), in intestinal epithelial cells (IECs). We found that TRPV1 was expressed by IECs and was intrinsically activated upon EGFR stimulation. Subsequently, TRPV1 activation inhibited EGFR-induced epithelial cell proliferation via activation of Ca2+/calpain and resulting activation of protein tyrosine phosphatase 1B (PTP1B). In a murine model of multiple intestinal neoplasia (
Petrus R. de Jong, Naoki Takahashi, Alexandra R. Harris, Jihyung Lee, Samuel Bertin, James Jeffries, Michael Jung, Jen Duong, Amy I. Triano, Jongdae Lee, Yaron Niv, David S. Herdman, Koji Taniguchi, Chang-Whan Kim, Hui Dong, Lars Eckmann, Stephanie M. Stanford, Nunzio Bottini, Maripat Corr, Eyal Raz
The prevalence of brain tumors in males is common but unexplained. While sex differences in disease are typically mediated through acute sex hormone actions, sex-specific differences in brain tumor rates are comparable at all ages, suggesting that factors other than sex hormones underlie this discrepancy. We found that mesenchymal glioblastoma (Mes-GBM) affects more males as the result of cell-intrinsic sexual dimorphism in astrocyte transformation. We used astrocytes from neurofibromin-deficient (
Tao Sun, Nicole M. Warrington, Jingqin Luo, Michael D. Brooks, Sonika Dahiya, Steven C. Snyder, Rajarshi Sengupta, Joshua B. Rubin
Activation of central PPARγ promotes food intake and body weight gain; however, the identity of the neurons that express PPARγ and mediate the effect of this nuclear receptor on energy homeostasis is unknown. Here, we determined that selective ablation of PPARγ in murine proopiomelanocortin (POMC) neurons decreases peroxisome density, elevates reactive oxygen species, and induces leptin sensitivity in these neurons. Furthermore, ablation of PPARγ in POMC neurons preserved the interaction between mitochondria and the endoplasmic reticulum, which is dysregulated by HFD. Compared with control animals, mice lacking PPARγ in POMC neurons had increased energy expenditure and locomotor activity; reduced body weight, fat mass, and food intake; and improved glucose metabolism when exposed to high-fat diet (HFD). Finally, peripheral administration of either a PPARγ activator or inhibitor failed to affect food intake of mice with POMC-specific PPARγ ablation. Taken together, our data indicate that PPARγ mediates cellular, biological, and functional adaptations of POMC neurons to HFD, thereby regulating whole-body energy balance.
Lihong Long, Chitoku Toda, Jing Kwon Jeong, Tamas L. Horvath, Sabrina Diano