Diabetes mellitus contribution to the remodeling of the tumor microenvironment in gastric cancer

Figure 1 Diabetes mellitus can sculpture the tumor microenvironment of gastric cancer through a myriad of different molecular mechanisms ranging from dysregulation of cellular signaling pathways to marked metabolic disturbances. TME: Tumor microenvironment; ECM: Extracellular matrix; miRNAs: MicroRNAs; CAFs: Cancer-associated fibroblasts; TAMCs: Tumor-associated mast cells; LOX: Lysyl oxidase; TGF-β: Transforming growth factor β; RAGE: Receptor of advanced glycation end products; AGE: Advanced glycation end product; ChREBP: Carbohydrate-responsive element-binding protein.

Figure 2 The molecular mechanisms involved in the contribution of diabetes mellitus to the remodeling of gastric cancer microenvironment determine crucial phenotypical changes not only on tumor cells but also in many other infiltrating cells. All changes may then result in a supporting tumor-growth niche that favors angiogenesis, invasion, and metastasis, as well as interference with anti-tumor immunity and thus generating more aggressive tumor phenotypes. ECM: Extracellular matrix.