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Abstract
<p id="d811025e151">Macroautophagy/autophagy is a well-established process involved
in maintaining cellular
homeostasis, but its role in cancer is complex and even controversial. Many studies
have reported a correlative relationship between increased autophagy and evolving
cancer cells under stress conditions such as nutrient or oxygen deprivation; however,
there has been a lack of a plausible mechanistic link to properly target the autophagy
process in the context of this microenvironment. We recently unveiled a positive regulatory
loop involving TGM2 (transglutaminase 2)-NFKB/NF-κB signaling, IL6 and autophagy in
cancer using mantle cell lymphoma (MCL) as a model system. These pathways are functionally
connected to each other, thereby promoting malignant B cell survival and leading to
enhanced lymphoma progression both in mice and in patients. Disruption of this network
could provide an opportunity to increase the efficacies of current therapies and to
reduce MCL drug resistance.
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[1
] Center for Stem Cell and Regenerative Disease, Brown Foundation Institute of Molecular
Medicine for the Prevention of Human Diseases (IMM), the University of Texas-Health
Science Center at Houston, Houston, TX USA