Cancer cells are exposed to a wide range of stress sources, such as nutrient deprivation and
hypoxia, as well as cytotoxic
chemotherapy and
radiotherapy. Certain forms of stress can also promote survival activating the metabolic autophagy pathway in
cancer cells. Autophagy is dramatically increased in
cancer cells. In these conditions, it is becoming evident that autophagy protects cells, by providing an alternative energy source and by eliminating dysfunctional organelles or
proteins. Its role in
tumorigenesis is more controversial and both the presence and the absence of autophagy have been implicated. Autophagy is known to be associated with the poor outcome of patients with various types of
cancers, and its effectiveness as a prognostic marker in
colorectal cancer was demonstrated by several studies. The inhibition of autophagy may be a potential therapeutic target in
colorectal cancer. In vitro experiments have shown that the inhibition of autophagy increases 5-FU-induced apoptosis. There are two trials currently investigating the addition of
chloroquine to 5-FU-based
chemotherapy and
bevacizumab. In the present study, we evaluated the expression of LC3B-II in samples of human colorectal microadenomas (i.e., dysplastic
aberrant crypt foci) and
carcinomas compared to normal mucosa. Furthermore, the expression pattern of LC3B-II was assessed in
carcinomas classified as
DNA microsatellite stable (MSS) and unstable (MSI). Thus, immunofluorescence techniques coupled with confocal microscopy and immunoblot experiments were performed. The results clearly showed a significant increase in expression of the autophagic key factor in microadenomas and
carcinomas with respect to normal mucosa. In MSS
carcinomas, the level of LC3B-II expression was higher than that in the MSI
carcinomas.