Anti-cancer drug molecules targeting cancer cell cycle and proliferation.

Cancer, a vicious clinical burden that potentiates maximum fatality for humankind, arises due to unregulated excessive cell division and proliferation through an eccentric expression of cell cycle regulator proteins. A set of evolutionarily conserved machinery controls the cell cycle in an extremely precise manner so that a cell that went through the cycle can produce a genetically identical copy. To achieve perfection, several checkpoints were placed in the cycle for surveillance; so, errors during the division were rectified by the repair strategies. However, irreparable damage leads to exit from the cell cycle and induces programmed cell death. In comparison to a normal cell, cancer cells facilitate the constitutive activation of many dormant proteins and impede negative regulators of the checkpoint. Extensive studies in the last few decades on cell division and proliferation of cancer cells elucidate the molecular mechanism of the cell-cycle regulators that are often targeted for the development of anti-cancer therapy. Each phase of the cell cycle has been regulated by a unique set of proteins including master regulators Cyclins, and CDKs, along with the accessory proteins such as CKI, Cdc25, error-responsive proteins, and various kinase proteins mainly WEE1 kinases, Polo-like kinases, and Aurora kinases that control cell division. Here in this chapter, we have analytically discussed the role of cell cycle regulators and proliferation factors in cancer progression and the rationale of using various cell cycle-targeting drug molecules as anti-cancer therapy.