ArticlebioRxiv : the preprint server for biology2025
Suppression of PP2A-B56α Drives EMT in EGFR Mutant Non-Small Cell Lung Cancer.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Lung cancer is the leading cause of cancer-related deaths in the United States and ∼50% of these patients present with metastatic disease at diagnosis. Epithelial-to-Mesenchymal Transition (EMT) is an important initiating step in the metastatic cascade that allows cells to acquire the migratory and invasive phenotypes necessary for dissemination. The transcriptional reprogramming that takes place during EMT has been well described in multiple cancer types; however, the posttranslational regulatory mechanisms that govern EMT are poorly understood. Protein Phosphatase 2A (PP2A) is serine/threonine (ser/thr) phosphatase that accounts for 50% of cellular ser/thr phosphatase activity and is critically important in regulating signaling homeostasis. PP2A dysregulation has been implicated in cell state regulation, EMT, and metastasis, but the roles of individual PP2A complexes are poorly understood. Our data indicate that suppression of the specific PP2A complex, PP2A-B56α, results in decreased expression of epithelial markers and increased expression of mesenchymal markers consistent with EMT. These molecular changes are associated with migratory and invasive phenotypes both
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