Abstract
Challenges in Cancer Molecular Targets and Therapeutics
Highlights
Most of the target-specific drugs have hitherto been designed to cripple proteins or molecular pathways that are thought to be the Achilles’ heel of cancer
Cancer cells become addictive to Hsp90 and proteasomal functions for survival as the latter are required to fold the misfolded oncoproteins, which otherwise will be destroyed through the ubiquitination-dependent proteasome degradation pathways (Whitesell and Lindquist, 2005)
The observation that cancer cells show increased rate of glycolysis can be traced back to as early as 1920s (Warburg, 1923). Increased glycolysis under both aerobic and anaerobic conditions promotes diversion from intracellular glucose to pyruvate, ATP, and NADH that in turn facilitate biosynthesis of nucleosides and amino acids required for rapid cancer cell growth and survival
Summary
Most of the target-specific drugs have hitherto been designed to cripple proteins or molecular pathways that are thought to be the Achilles’ heel of cancer. In the recent past, targeting addictive oncoproteins, such as receptor tyrosine kinases, has overwhelmingly led drug development in the field of cancer targetspecific therapies. A major challenge in this field will be to identify the right cancer patients whose cancer cell survival is Hsp90- or proteasome-dependent, and to hit the targets right and hard in time with those inhibitors.
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