Cyclin Dependent Kinase (CDKs) regulates cell cycle commitment and DNA synthesis. Cell division in mammalian cells is driven by protein kinase that regulates progression through the various phases of cell cycle. The activity of cyclins and their associated CDKs are frequently deranged in human cancers. For this reason, Cyclin-CDK complexes have been considered as very promising therapeutic targets in human malignancies. An obvious concern whether, blocking cyclin-CDK function would preferentially affects cancer cells but not normal and non-transformed cells. The cell cycle represents a series of tightly integrated events that allow the cell to grow and proliferate. Critical part of the cell cycle machinery is the CDK, which, when activated, provide a means for the cell to move from one phase of the cell cycle to next. The cell cycle also serves to protect the cell from DNA damage. Thus, cell cycle arrest represents a survival mechanism that provides tumour cell, to repair its own damaged DNA Thus, abrogation of cell cycle checkpoints, before DNA repair is complete can activate the apoptotic cascade leading to cell death. Misregulation of CDK is one of the most frequent alterations in human cancer. CDK are critical regulators of cell cycle progression and RNA transcription. A series of targeted agents that directly inhibit the CDKs, inhibit unrestricted cell growth, and induce growth arrest. Recent attention has also focused on these drugs as inhibitors of transcription. In this review we are summarizing that why CDK is important target for cancer chemotherapy and why finding out the best and potent kinase inhibitor is essential.
Keywords: Cancer, CAK, Cell cycle, CDK, Cyclin, Kinases, Phosporylation, Threonine