ReviewFrontiers in cell and developmental biology2026
PI3K/AKT/mTOR signaling at the immune checkpoint interface in lung cancer: molecular mechanisms, Tumor-Immune remodeling, therapeutic resistance, and emerging treatment strategies.
Review in Frontiers in cell and developmental biology, 2026. 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
Immune checkpoint inhibitors targeting the PD-1/PD-L1 axis have substantially improved the treatment of lung cancer, yet durable responses remain limited by primary and acquired resistance. Increasing evidence identifies the PI3K/AKT/mTOR pathway as a central link between oncogenic signaling, metabolic adaptation, and tumor immune suppression. Genetic and molecular alterations, including PIK3CA activation, PTEN loss, and aberrant EGFR or ALK signaling, can activate this pathway and regulate PD-L1 expression at transcriptional, translational, and post-translational levels. Conversely, tumor-intrinsic PD-L1 signaling can reinforce PI3K/AKT/mTOR activity, promoting proliferation, survival, glycolysis, epithelial-mesenchymal transition, and resistance to therapy. This reciprocal interaction establishes a feedforward circuit that supports lung cancer progression and immune escape. The pathway also reshapes the tumor microenvironment by promoting regulatory T-cell expansion, M2-like macrophage polarization, myeloid-cell recruitment, CD8
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