Functionally, MYCL overexpression suppresses androgen receptor signaling, induces neuroendocrine-like transcriptional reprogramming, and remodels cytoskeletal and adhesion pathways associated with cellular plasticity, whereas MYCL knockdown disrupts neuroendocrine lineage identity and restores adenocarcinoma-associated gene expression, including MYC. Here, AR is linked to adenocarcinoma.