Cancer cells are characterized by a high glycolytic rate, which leads to energy regeneration and anabolic metabolism; a consequence of this is the abnormal expression of pyruvate kinase isoenzyme M2 (PKM2). Multiple studies have demonstrated that the expression levels of PKM2 are upregulated in numerous cancer types. Consequently, the mechanism of action of certain anticancer drugs is to downregulate PKM2 expression, indicating the significance of PKM2 in a chemotherapeutic setting. Furthermore, it has previously been highlighted that the downregulation of PKM2 expression, using either inhibitors or short interfering RNA, enhances the anticancer effect exerted by THP treatment on bladder cancer cells, both in vitro and in vivo. The present review summarizes the detailed mechanisms and therapeutic relevance of anticancer drugs that inhibit PKM2 expression. In addition, the relationship between PKM2 expression levels and drug resistance were explored. Finally, future directions, such as the targeting of PKM2 as a strategy to explore novel anticancer agents, were suggested. The current review explored and highlighted the important role of PKM2 in anticancer treatments.
Keywords: PKM2; cancer; chemotherapeutic drugs; resistance; target.
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