Cell proliferation and carcinogenesis may share a common basis of permeable plasma membrane clusters.
Wound potentials increase the surface potential of exposed areas of nearby cells. In these cells, soluble cytoplasmic bases are assumed gradually to move nearer the exposed area. Acidic molecules on the cell surface migrate to points opposite the bases. The image-charged species are mutually attracted to form transmembrane clusters. At clusters, membrane permeability increases and the cell is stimulated to cycle. When the wound heals, its clusters disperse, leaving a small 'permanent' residuum. Permanent clusters initiate cells to malignancy. They have (or develop) lipophilic molecules on both surfaces that help fix them in the membrane. Exposed cells contaminated with polycyclic aromatic hydrocarbon carcinogens (PAH) readily form permanent clusters. At mitosis, clusters on parental plasma membrane pass with that membrane to a daughter cell. Promotion results from many short-term or a single long-term exposure of initiated membranes to abnormal surface charge. Permanent clusters increase on the membrane after repeated wounding, proximity of charged foreign bodies like plastic film or asbestos, or oxidation of surface molecules. Progression requires acceleration of cluster growth so the daughter cell membranes become as leaky at maturity as was the parent membrane. One mechanism suggested involves reversible phosphorylation by membrane-bound kinases; another involves attraction of a basic protein (p36) to the membrane.
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D000818:Animals; D002455:Cell Division; D002462:Cell Membrane / Q000502:physiology; D002463:Cell Membrane Permeability; D002471:Cell Transformation, Neoplastic; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D009374:Neoplasms, Experimental / Q000473:pathology / Q000503:physiopathology; D009857:Oncogenes; D014947:Wounds and Injuries / Q000503:physiopathology