Abstract

Methylthioadenosine Phosphorylase is a well-known tumor suppressor and a regulator for purine and pyrimidine synthesis and metabolism. Several previous studies show MTAP could be a prognostic marker independent or coordinate with p16 in multiple cancer types. Furthermore, inhibitors of MTAP have been developed and tested in in vitro and in vivo experiment to support the selective tumor cell-killing theory of MTAP. The review aims to provide a deep understanding of the clinical role and the metabolic reprogramming regulated by MTAP in cancer as the guide to found out and solve the problems of MTAP based cancer therapy.

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