Abstract
Recent exome-sequencing efforts have revealed that the MGA gene, which encodes a heterodimeric partner of the MYC-interacting protein MAX, is significantly mutated (∼8%) in lung adenocarcinomas. Most MGA mutations are loss-of-function, suggesting that MGA may act as a tumor suppressor. MGA mutations are mutually exclusive to MYC gene amplification, suggesting the involvement of MGA in the MYC pathway. Here, we aimed to characterize both the cellular and molecular role of MGA in lung adenocarcinoma, with a focus on studying its role in modulating the MYC pathway.
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