Tailoring of chitosan through the involvement of its amino, acetamido, and hydroxy groups can give derivatives of enhanced solubility and remarkable anticancer activity. The general mechanism of such activity is associated with the disturbances in normal functioning of cell cycle, interference to the central dogma of biological system from DNA to RNA to protein or enzymatic synthesis, and the disruption of hormonal path to biosynthesis to inhibit the growth of cancer cells. Both chitosan and its various derivatives have been reported to selectively permeate through the cancer cell membranes and show anticancer activity through the cellular enzymatic, antiangiogenic, immunoenhancing, antioxidant defense mechanism, and apoptotic pathways. They get sequestered from noncancer cells and provide their enhanced bioavailability in cancer cells in a sustained release manner. This review presents the putative mechanisms of anticancer activity of chitosan and mechanistic approaches of structure activity relation upon the modification of chitosan through functionalization, complex formation, and graft copolymerization to give different derivatives.

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Chitosan oligosaccharide and high molecular weight crab shell chitosan were functionalized as imidazole-2-carboxaldehyde chitosan thiosemicarbazones and their copper(II) complexes were synthesized. The synthesized compounds were characterized by FT-IR, 13C NMR, EPR spectroscopy, powder X-ray diffraction (PXRD) analysis, elemental analysis and magnetic susceptibility measurements. The low molecular weight chitosan thiosemicarbazones showed higher in vitro inhibitory activity as studied by MTT assay against the tumorigenic epithelial Madin-Darby Canine Kidney (MDCK) cell line than the corresponding high molecular weight chitosan derivative. The antitumorigenic enhancement upon the complex formation was revealed by the better inhibitory activity of copper(II) chitosan thiosemicarbazone chelates.