Targeting Autophagy for Pituitary Tumors

Abstract

Pituitary tumors, arising from the pituitary gland, can be classified as functioning or non-functioning based on their hormone production. Previous studies demonstrated that impairment of cellular processes, such as autophagy, a crucial cellular recycling mechanism, has been implicated in pituitary tumorigenesis and hormone dysregulation. This review comprehensively examines the intricate relationship between autophagy and pituitary tumors. We explore the multifaceted role of autophagy in cancer, highlighting its dual nature as both a tumor suppressor and a promoter depending on the context. We also discuss the specific mechanisms of autophagy, including macroautophagy, mitophagy, crinophagy, and their relevance to pituitary tumorigenesis and hormone regulation. Furthermore, we analyze the current literature regarding the impact of various therapeutic interventions in pituitary tumor cells, with both autophagy-promoting and autophagy-inhibiting strategies. We address the challenges in interpreting autophagy activity and its complex interplay with hormone production. Current evidence suggests the potential of targeting autophagy as a therapeutic approach for pituitary tumors, emphasizing further research and clinical trials to determine the optimal strategy for individual patients and improve long-term outcomes.

Keywords: autophagy; cell proliferation; hormone production; pituitary tumors.

Figure 1

Double-role autophagy in pituitary tumor pathogenesis. Autophagy-mediated pituitary tumorigenesis: Under specific conditions, autophagy can facilitate pituitary tumor growth and hormone production. Mechanisms include: supplying amino acids and metabolic substrates through the degradation of cellular components, supporting increased energy demands of rapidly proliferating tumor cells, enhancing signals for cellular proliferation and synthesis of secretory molecules, including peptide hormones. Autophagy-mediated pituitary tumor suppression: Conversely, autophagy can also exert tumor-suppressive effects. This can occur through: selective degradation of oncogenic proteins or damaged organelles, preventing their accumulation and mitigating pro-tumorigenic signaling, sustaining signals for cellular proliferation and synthesis of secretory molecules, leading to decreased hormone secretion, and potentially limiting tumor growth. Otherwise, excessive or unrestricted autophagy leads to cell death. The balance between these opposing functions of autophagy is likely determined by the specific genetic and microenvironmental context of the pituitary tumor.