Alkaloids, nitrogen-containing compounds, are found in living organisms ranging from microbes to seed-producing plants all over the world. About more than 20,000 alkaloids have been discovered, mostly occurring in higher plants of the families Ranunculaceae, Papaveraceae, Leguminosae, Loganiaceae and Menispermaceae. These compounds are able to inhibit cancer proliferation, especially gastrointestinal cancer, which constitutes the highest incidence rate all over the world. The most diversified group of phytochemicals, alkaloids offer a mighty series of chemical scaffolds and moieties which can be harnessed to ameliorate the devastating consequences underlying cancer. Gastrointestinal (GIT) cancers constitute the malignancies of esophageal, gastric, pancreatic, colorectal and anal tumors, which possess aberrant metabolic signals giving rise to uncontrolled cell proliferation. These cancers are the most frequent of all cancers and account for the high mortality rates worldwide. Conventional therapeutic options carry the risks like being non-economical as well as they possess severe side effects. Natural products offer a wide spectrum of pharmacological properties which can overcome these risk factors by providing cheaper products and are reliable regarding their bio-safety profiles. Alkaloids can be investigated in detail to investigate their pharmacological potential against GIT cancers. Several alkaloids are known to modulate the cell signaling pathways by inducing cell cycle arrest at G0/G1, S and G2/M phases in addition to being the apoptosis inducers. In addition to that, they are also known to target various metabolic pathways, such as p53, β-catenin, MAPK and PIM3. The chapter intends to investigate the biological as well as pharmacological profiles of various alkaloids with special reference to GIT cancers in order to update scientists and researchers about the pharmaceutical potential of these compounds.
Keywords: Alkaloids, Cell cycle arrest, Clinical potential, Gastrointestinal cancer, GIT cancers, Modulation of singling pathways.
