Endocrine Crosstalk: Diabetes as a Catalyst for Cancer Progression and Metastasis
Diabetes and cancer represent two of the most pervasive and challenging health crises worldwide, with a growing body of evidence revealing a profound and complex interplay between these diseases. Beyond being a mere comorbidity, diabetes acts as a potent catalyst in cancer progression and metastasis, driven primarily by the endocrine and metabolic disruptions characteristic of hyperglycemia and hyperinsulinemia. Chronic elevations in glucose and insulin levels foster a tumor-promoting microenvironment that accelerates cancer cell proliferation, survival, migration, and angiogenesis. This review synthesizes current understanding of the molecular and cellular mechanisms linking diabetes to cancer, emphasizing the pivotal roles of advanced glycation end products (AGEs), the AGE–RAGE signaling axis, insulin resistance, and inflammatory pathways. Moreover, we explore the emerging influence of the gut microbiome in modulating metabolic and oncogenic processes common to both diseases. Epidemiological data underscore the heightened cancer risk and mortality observed in diabetic patients, particularly for pancreatic, liver, colorectal, and breast cancers, while highlighting the need for integrated clinical strategies. By unraveling the endocrine crosstalk that connects diabetes and cancer, this review aims to illuminate potential therapeutic targets and inspire novel dual-action interventions that may curb the dual burden of these interlinked diseases.
Keywords: Diabetes, Metastasis, Cancer progression, Hyperglycemia, Hyperinsulinemia.
