Compartmentalization Modules of Inflammatory Response are Centered on the Epithelial-Mesenchymal Transition of Transforming Cells in Carcinogenesis

Abstract

The epithelial-mesenchymal transition (EMT) event in carcinogenesis is dependent on multiple operant pathways of master transcription as proposed for NF-kappaB and in terms of the initiated progression of malignant transformation. Inflammation is a primarily compartmentalized series of distinct and overlapping systems that induce and enhance multifocal operabilities within both the nucleus and cytoplasm by systems of enhancer/inhibitory modes of modulation of multi-gene transcription. In terms therefore of a compensatory system of response, carcinogenesis includes a series of steps in characterization of nuclear/cytoplasmic duality targeting ultimately the emergence of tumor cell invasiveness as the epithelial-mesenchymal transition. Emergence of such transition is hallmark for carcinogenesis within contexts of aberrant cell proliferation and anti-apoptosis as exerted by NF-kappaB proinflammation. NF-kB is the main transcription factor that regulates the expression of inflammation-related genes and is in turn influenced by autophagy; also autophagy interacts with inflammation in numerous disease states. It is relevant; in addition, that NF-kB participates in the release of inflammatory cytokines in patients with sepsis with pathogenic implications of sepsis in carcinogenesis.