Editor-in-Chief: Francis J. Castellino Kleiderer-Pezold Professor of Biochemistry Director, W.M. Keck Center for Transgene Research Dean Emeritus, College of Science 230 Raclin-Carmichael Hall, University of Notre Dame Notre Dame, IN 46556 USA
Affiliation: 2nd Department of Internal Medicine, Semmelweis University, H-1088 Budapest, Szentkiralyi street 46. Hungary.
Accumulating evidence indicates that the aberrantly altered process of autophagy is definitely involved in carcinogenesis. Nonetheless, Toll-like receptors (TLRs) sensing cell-derived pattern/danger-associated molecules also have the capacity to promote tumor development and immune escape. TLRs are usually expressed in immunocompetent cells, though several types of cancer cells have also been reported to display these innate immune receptors. On the other hand, however, both TLR- and autophagy-related signals may exert tumor suppressor mechanisms mainly in a cell-specific and context-dependent manner. The role of autophagy has been radically expanded, and now this machinery is considered as a fundamental eukaryotic cellular homeostatic process and integral component of the immune system influencing infection, inflammation and immunity. Recent studies have documented that TLRs and autophagy are interrelated in response to danger signals, furthermore there is a controling cross-talk among them to avoid deficient or excessive immunological effects. Although the potential interaction of autophagy and TLRs in cancer cells has not yet been clarified, it seems to be a critical aspect of cancer development and progression. Upon translation of basic knowledge into practice it is reasonable to speculate that modulation of the TLR-autophagy regulatory loop might be relevant for cancer treatment by providing further possible therapeutic targets.