| Most commonly recognized as a catabolic pathway, autophagy is a
perplexing mechanism through which a living cell can free itself of
excess cytoplasmic components, i.e., organelles, by means of certain
membranous vesicles or lysosomes filled with degrading
enzymes. Upon exposure to external insult or internal stimuli, the
cell might opt to activate such a pathway, through which it can gain
control over the maintenance of intracellular components and thus
sustain homeostasis by intercepting the formation of unnecessary
structures or eliminating the already present dysfunctional or inutile
organelles. Despite such appropriateness, autophagy might also be
considered a frailty for the cell, as it has been said to have a rather
complicated role in tumorigenesis. A merit in the early stages of
tumor formation, autophagy appears to be salutary because of its
tumor-suppressing effects. In fact, several investigations on tumorigenesis
have reported diminished levels of autophagic activity in
tumor cells, which might result in transition to malignancy. On the
contrary, autophagy has been suggested to be a seemingly favorable
mechanism to progressed malignancies, as it contributes to
survival of such cells. Based on the recent literature, thismechanism
might also be activated upon the entry of engineered nanomaterials
inside a cell, supposedly protecting the host from foreign materials.
Accordingly, there is a good chance that therapeutic interventions
for modulating autophagy in malignant cells using nanoparticles
may sensitize cancerous cells to certain treatment modalities, e.g.,
radiotherapy. In this review, we will discuss the signaling pathways
involved in autophagy and the significance of the mechanism itself
in apoptosis and tumorigenesis while shedding light on possible |