Insulin resistance has been studied extensively at systemic, organ, tissue and cellular and molecular levels. Overnutrition plays an essential role in the development of chronic metabolic diseases such as obesity and type 2 diabetes. For subjects without genetic defects, the development of insulin resistance and type 2 diabetes is a graduate process. How the transition from an insulinsensitive state to an insulin-resistant state occurs, and what the roles of nutrients are in the process have not been fully understood. Here, we try to summarize the current understanding of insulin-regulate gene expression in the liver, and describe a phenomenon of hepatic insulin resistance at gene expression (HIRAGE), which may be linked to overnutrition.

Epithelial-mesenchymal transition (EMT), a lineage transition from epithelium to mesenchyme, is induced by a convergence of signaling pathways and often driven by TGFß/SMAD signaling. Except for its critical roles on cell shape and motility during cancer invasion and metastasis, TGFß/SMAD activation-induced EMT has also been reported to be involved in cancer stem cell (CSC) generation.

Pancreatic cancer is one of the most lethal solid tumor malignancies and it is projected to become a leading cause of cancer related deaths in coming years. It is often diagnosed at an advanced stage owing to the lack of specific symptoms and rapid invasion.

Epigenetic processes provide a mechanism for integrating metabolic inputs and translating them into various phenotypic outputs [1,2]. Indeed, epigenetic modifiers often require or are inhibited by key citric acid cycle (CAC) metabolites (e.g. succinate,

Inflammation drives prostate cancer (PCa) progression. While inflammation is a cancer hallmark, the underlying mechanisms mediating inflammation-induced PCa are still under investigation. Interleukin-1 (IL-1) is an inflammatory cytokine that promotes cancer progression, including PCa metastasis and castration resistance. We previously found that acute IL-1 exposure represses PCa androgen receptor (AR) expression concomitant with the upregulation of pro-survival proteins, causing de novo accumulation of castration-resistant PCa cells.