Abstract
Autophagy is a conserved and tightly regulated cellular catabolic process that involves the lysosomal degradation pathway. Intracellular recycling of macromolecules and organelles provided by autophagy is an integral part of normal cellular function and permits cells survival under starvation conditions, maintaining cell growth and the homeostasis of organisms. In addition to its normal role in cell physiology, auto- phagy is closely linked to both tumorigenesis and cancer cell response to treatments. In fact, anticancer drugs can induce autophagy but it remains contro- versial whether this process leads to cancer cell death or protects cancer cells from cellular stress. The role of autophagy in cancer is complex and is likely dependent on tumor type, stage, and genetic context. However, recent evidences demonstrate a tight interconnection of autophagy with several cell death pathways and reveal an active contribution of auto- phagy to cell death. When autophagy is directly in- volved in the death process, the cell death process is designated “autophagic cell death” (ACD). In this review, we will give a comprehensive overview of the autophagic signaling pathway, its role and regulation in cancer cells; moreover, we will try to define the molecular mechanisms at the basis of the autophagic cell death showing that PPAR-γ activation plays a role in the induction of autophagy in cancer cells.
Highlights
In multicellular organisms, the number of cells is determined by a tightly regulated balance between their proliferation and their death
We will give a comprehensive overview of the autophagic signaling pathway, its role and regulation in cancer cells; we will try to define the molecular mechanisms at the basis of the autophagic cell death showing that Peroxisome proliferator activated receptors (PPARs)-γ activation plays a role in the induction of autophagy in cancer cells
In contrast with the necrosis, apoptosis represents a physiological mechanism of programmed cell death, which ensures the elimination of cells that have completed their life cycle, or that, as a result of genetic damage, have become useless or harmful to the organism [2]
Summary
The number of cells is determined by a tightly regulated balance between their proliferation and their death. In particular: autophagy, or lysosomal cell death, is an important process in the preservation of cytoplasmic homeostasis, which gives form to the selective elimination of cytoplasmic material and organelles sequestered in autophagic vacuoles of lysosomal nature It is possible this mechanism is able to modulate the intracellular stores of functional mitochondria, and that it is able to influence events dependent on the mitochondrial activity, such as apoptosis [6]. -Mitotic catastrophe is characterized by multiple nuclear fragmentation; is a process independent of caspases and leads to the activation of certain molecules involved in cell cycle regulation as cdk 1. It is characterized by aberrant activation of mitosis; the cell rather than to divide itself runs into death, it fragments and dies
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