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PI3K/AKT signaling pathway: molecular crossroads in tumorigenesis and therapeutic innovation

Aug 2026 · Signal Transduction and Targeted Therapy · Vol 11 · 0 citations · 479 references
Medicine

TL;DR

This study comprehensively investigates PI3K/AKT signaling, elucidating its involvement across diverse human systemic tumors and analyzing the interplay between this pathway and other signaling cascades implicated in tumorigenesis.

Abstract

The PI3K/AKT signaling pathway serves as a pivotal regulatory hub that governs essential cellular processes, including growth, proliferation, metabolism, survival, and migration. In the context of tumorigenesis and cancer development, aberrant activation of this pathway drives malignant transformation, enhances invasive and metastatic potential, and confers resistance to therapeutic interventions, ultimately resulting in tumor progression and poorer clinical outcomes. This study comprehensively investigates PI3K/AKT signaling, elucidating its involvement across diverse human systemic tumors and analyzing the interplay between this pathway and other signaling cascades implicated in tumorigenesis. Emphasis is placed on mechanistic insights into the role of the PI3K/AKT pathway in tumor initiation and progression across various systems, alongside an overview of therapeutic strategies targeting PI3K/AKT signaling. Notably, advances in research on the PI3K/AKT pathway have identified a wide array of potential therapeutic targets, facilitating significant progress in related treatment modalities. Given the extensive involvement of PI3K/AKT signaling in diverse biological processes, optimizing the therapeutic efficacy of PI3K/AKT-targeted interventions while minimizing associated adverse effects remains a critical challenge, necessitating innovative approaches for substantial therapeutic breakthroughs. Therefore, a systematic and nuanced understanding of the pathway’s role in tumor biology is essential for advancing foundational research and informing future clinical developments in this field.

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