THE INTERRELATIONSHIP BETWEEN APOPTOSIS AND AUTOPHAGY PROCESSES AND THEIR IMPACT ON TUMOR CELL PROLIFERATION

This article examines the complex molecular interrelationship between apoptosis and autophagy and how their coordinated or antagonistic regulation influences tumor cell proliferation. Apoptosis, a caspase-dependent programmed cell death pathway, is frequently impaired in cancer, enabling malignant cells to evade death signals. Autophagy, a lysosomal degradation and recycling mechanism, plays a dual role: suppressing early tumorigenesis while supporting survival in established tumors under metabolic or therapeutic stress. The paper analyzes shared regulatory nodes including Beclin-1, Bcl-2 family proteins, p53, mTOR, AMPK, and PI3K/Akt pathways, which integrate stress responses and determine cell fate. Special attention is given to how tumor cells exploit autophagy to escape apoptosis, contributing to treatment resistance, sustained proliferation, and cancer stem-cell survival. Understanding these mechanisms provides a foundation for therapeutic strategies targeting both pathways to enhance anticancer efficacy.

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