SECONDARY METABOLISM OF LICHENS AS THE CYTOTOXIC AGENT TO KILL THE CANCER CELLS

Abstract

Abstract

Cancer is competing with cardiovascular diseases to rank as the number one cause of fatality worldwide. The distinctive nature of cancer cells is to grow and multiply regardless of the inhibitory signals to avoid apoptosis.  Lichens are organisms formed from a combination of fungus and algae or cyanobacteria, and these components are in a mutual relationship. Lichens produce primary and secondary metabolites and hormones due to environmental changes or infection. These metabolites have an essential role in protecting the plants from exogenous invaders. For this reason, these creatures can survive drastic environmental changes and severe infections. Over the years, many researchers have tested the secondary metabolites in vivo and in vitro and found promising antitumor, antifungal, antiviral, antibacterial, and antipyretic properties. These beneficial activities were enticing to many pharmaceutical companies. These secondary metabolites can be classified according to their biochemical structure, biosynthetic pathway, and maturation. In this particular study, we are focusing on the structure of Lichen secondary metabolites, biosynthesis, and anticancer activity. Secondary metabolites can inhibit carcinogenesis by targeting multiple stages of growth and angiogenesis signaling mechanisms and induction of apoptosis and autophagy in tumor cells. The programmed cell death is induced by activating mTOR and JNK signaling pathways and promotes the expression of p53, p38, Bax, and cleaved PARP genes. At the same time, autophagic tumor cell death is instigated by stimulation of the LC3II protein. On the other hand, secondary metabolites activate cell cycle arrest by hindering cyclin-dependent kinases 2, 4, cyclin D1, cyclin B1, and Cdc25C gene expression. Lichen increases the production of reactive oxygen species, which causes suppression of tumor cells by negatively regulating the biosynthesis of ATP and nucleotides. Secondary metabolites provoke the immune response against cancer cells.  Clinically, despite the evolution of cancer medicines, a wide range of complications are documented.