Abstract
For the last couple of decades, natural products, either applied singly or in conjunction with other cancer therapies including chemotherapy and radiotherapy, have allowed us to combat different types of human cancers through the inhibition of their initiation and progression. The principal sources of these useful compounds are isolated from plants that were described in traditional medicines for their curative potential. Leelamine, derived from the bark of pine trees, was previously reported as having a weak agonistic effect on cannabinoid receptors and limited inhibitory effects on pyruvate dehydrogenase kinases (PDKs). It has been reported to possess a strong lysosomotropic property; this feature enables its assembly inside the acidic compartments within a cell, such as lysosomes, which may eventually hinder endocytosis. In this review, we briefly highlight the varied antineoplastic actions of leelamine that have found implications in pharmacological research, and the numerous intracellular targets affected by this agent that can effectively negate the oncogenic process.
Highlights
Cancer remains a major cause of mortality on a global scale
When trapped in the lysosome, and not available for cellular processes, autophagic flux and receptor-mediated endocytosis are inhibited [62,63], which is associated with the inhibition of receptor tyrosine kinases RTK signaling pathways, which can suppress the activation of the downstream PI3K/AKT, STAT3, and MAPK signaling cascades [4,28] that are responsible for cancer progression
Highlighted that leelamine decreased the proliferation and vascular development of melanoma cancer cells and increased apoptosis by initiating programmed cell death mediated through a G0–G1 block and causing fewer cells to assemble in the S-phase of the cell cycle. Those observations were induced by the inhibition of the PI3K/Phosphorylated Protein kinase B. Bcl-2 (Akt), MAPK, and STAT3 pathways through the suppression of intracellular cholesterol transport, and similar effects were noted in preclinical models
Summary
Myriam Merarchi 1,2 , Young Yun Jung 3 , Lu Fan 2 , Gautam Sethi 2, * and Kwang Seok Ahn 3, *. College of Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea
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