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TP53 is a critical tumor suppressor that is mutated in approximately 50% of human cancers. Unveiling the downstream target genes of TP53 that fulfill its tumor suppressor function is an area of intense investigation.  Zmat3  (also known as  Wig-1  or  PAG608 ) is one such downstream target of p53, whose loss in hemopoietic stem cells lacking the apoptosis and cell cycle regulators, Puma and p21, respectively, promotes the development of leukemia. The function of Zmat3 in tumorigenesis however remains unclear. Here, to investigate which oncogenic drivers co-operate with  Zmat3  loss to promote neoplastic transformation, we utilized  Zmat3  knockout mice in models of  c-MYC -driven lymphomagenesis and  Kras  G12D -driven lung adenocarcinoma development. Interestingly, unlike loss of  p53 ,  Zmat3  germline loss had little impact on the rate of tumor development or severity of malignant disease upon either the  c-MYC  or  Kras  G12D  oncogenic activation. Furthermore, loss of  Zmat3  failed to rescue  Kras  G12D  primary lung tumor cells from oncogene-induced senescence. Taken together, we conclude that in the context of  c-MYC- driven lymphomagenesis or mutant  Kras  G12D -driven lung adenocarcinoma development, additional co-occurring mutations are required to resolve Zmat3 tumor suppressive activity.

Consequences of Zmat3 loss in c-MYC- and mutant KRAS-driven tumorigenesis