Autophagy (AP) is a cell recovery programme that plays a critical role by
degrading dysfunctional organelles and misfolded proteins. Besides its position to
maintain homeostasis, the contribution of AP to the development and progression of
several pathological conditions, including cancer has been denoted. A significant
number of findings indicate the involvement of AP-mediated cell survival in the
progression of many tumors. However, the data in esophageal cancer (EC) appears to
be less initiated. In this chapter, first definition, types and mechanisms of AP are
described, and the following sections are focused on giving a clear view of the findings
that communicate AP with oncogenesis and tumor progression in EC. Moreover, the
use of several drugs, which are known to modulate AP (inhibitors [3-MA, Bafilomycin
etc.] and inducers [Nimotuzumab etc.]) in the treatment of EC, is discussed.
The current data indicated that although the role of AP in carcinogenesis, tumor
behavior and response to treatment in EC is non-negligible, the first problem to be
resolved is to determine whether AP should be stimulated or inhibited because it seems
that both strategies are encouraging. Another problem is the identification of the patient
who will benefit from the manipulation of AP. Finally; the use of existing drugs that
may have off-target effects warrants the development of specific AP modulating
compounds suitable for use in patients with EC. The potential role of AP in EC
chemoresistance necessitates further investigations not only with AP related proteins
but also their related pathways into open up new corners for therapeutic intervention.
Keywords: Apoptosis, autophagosome, autophagy, Beclin-1, cancer, carcinogenesis,
cell survival, chemoresistance, esophageal carcinoma, esophagus, inhibition
of autophagy, LC3 protein, pathway, regulation of autophagy, treatment.
