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Colchicine is a medication used to prevent and treat gout, [3] [4] to treat familial Mediterranean fever [5] and Behçet's disease, [6] and to reduce the risk of myocardial infarction. [7] The American College of Rheumatology recommends colchicine, nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids in the treatment of gout.
While colchicine is not used to treat cancer in humans, it is commonly used to treat acute attacks of gout. [26] Colchicine is an anti-inflammatory drug that has been in continuous use for more than 3000 years. Colchicine is an oral drug, known to be used for treating acute gout and preventing acute attacks of familial Mediterranean fever (FMF).
Colchicine interferes with the inflammatory process by altering several important steps in the pathway. Microtubules are structural components of the cytoskeleton that lengthen and shrink for important cell functions. Colchicine binds to β- tubulin and forms tubulin-colchicine complexes.
Vinorelbine, Nocodazole, vincristine, and colchicine have the opposite effect, blocking the polymerization of tubulin into microtubules. Eribulin binds to the (+) growing end of the microtubules. Eribulin exerts its anticancer effects by triggering apoptosis of cancer cells following prolonged and irreversible mitotic blockade.
Cytoskeletal drugs are small molecules that interact with actin or tubulin.These drugs can act on the cytoskeletal components within a cell in three main ways. Some cytoskeletal drugs stabilize a component of the cytoskeleton, such as taxol, which stabilizes microtubules, or Phalloidin, which stabilizes actin filaments.
Colchicine arrests cells in metaphase and is a microtubule poison preventing mitotic spindle formation, much like nocodazole. It works by depolymerizing tubulin in microtubules, blocking progression to anaphase through sustained arrest at the spindle assembly checkpoint .
It is closely related to the natural alkaloid colchicine with the replacement of the acetyl group on the amino moiety with methyl, but it is less toxic. It depolymerises microtubules and limits microtubule formation (inactivates spindle fibre formation), thus arresting cells in metaphase and allowing cell harvest and karyotyping to be performed.
Using drugs such as nocodazole and colchicine, the mitotic spindle disassembles and the cell cycle is blocked at the metaphase-to-anaphase transition. Using these drugs (see the review from Rieder and Palazzo in 1992 [ 6 ] ), the putative control mechanism was named Spindle Assembly Checkpoint (SAC).