Table 1_LAPTM4B in tumor immune evasion: lysosomal autophagy, metabolic adaptation, and therapeutic resistance.docx

In this framework, LAPTM4B may contribute to sustained autophagic flux under stress, support metabolic conditions compatible with aerobic glycolysis, and potentially facilitate downstream immunosuppressive processes, including lactate-associated microenvironmental remodeling. We also review structural heterogeneity of LAPTM4B, clinical associations across multiple malignancies, multidrug-resistance mechanisms, and emerging evidence for EGFR-TKI escape mediated by LAPTM4B-dependent stabilization of ATP1A1 in non-small cell lung cancer.</p>Conclusions<p>Current evidence supports LAPTM4B as an important regulator of lysosomal adaptation and therapy resistance, whereas its broader role in tumor immune evasion remains a testable model rather than an experimentally settled mechanism.

We therefore present the autophagy-metabolism-immunity axis as a layered framework: experimentally supported in selected tumor contexts, indirectly supported by related metabolic and immune observations, and hypothesis-generating where direct causal evidence remains absent.</p>