Abstract
Autophagy as a primary homeostatic and catabolic process is responsible for the degradation and recycling of proteins and cellular components. The mechanism of autophagy has a crucial role in several cellular functions and its dysregulation is associated with tumorigenesis, tumor–stroma interactions, and resistance to cancer therapy. A growing body of evidence suggests that autophagy is also a key regulator of the tumor microenvironment and cellular immune response in different types of cancer, including colorectal cancer (CRC). Furthermore, autophagy is responsible for initiating the immune response especially when it precedes cell death. However, the role of autophagy in CRC and the tumor microenvironment remains controversial. In this review, we identify the role of autophagy in tumor microenvironment regulation and the specific mechanism by which autophagy is implicated in immune responses during CRC tumorigenesis and the context of anticancer therapy.
Highlights
Colorectal cancer (CRC) is the third most frequently diagnosed malignancy and the second leading cause of cancer-related deaths in the U.S.A. and worldwide [1]
Autophagy has been strongly associated with tumorigenesis in colorectal cancer
It is well known that tumors are characterized by a highly heterogeneous population of cancer, mesenchymal, immune, and stromal cells in a complex structure, which is identified as the tumor microenvironment
Summary
Colorectal cancer (CRC) is the third most frequently diagnosed malignancy and the second leading cause of cancer-related deaths in the U.S.A. and worldwide [1]. Autophagy is a major mechanism which is strongly associated with tumorigenesis in different types of cancer, including CRC. Like Beclin-1, LC3, ATG5, and ATG6, have a crucial role for autophagy from normal function to CRC, where these genes have been reported with high expression. Cancer cells of KRAS-dependent tumors use autophagy in order to support the growth of cancer cells under stressful conditions in hypoxic regions of tumors [8] All these studies highlight the dual role of autophagy as a tumor promoter or tumor suppressor mechanism. The increasing levels of autophagy, in these regions, are strongly associated with the regulation of the immune response in the tumor microenvironment [11,25]. Autophagy may be a promising therapeutic target in combination with other anti-neoplastic drugs and immunotherapy in the context of this unique cellular composition of the tumor microenvironment
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