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Background: Mitochondrial dysfunction is associated with neuronal disorders, and mitochondrial dynamics are altered in neurodegenerative diseases. Results: Inhibition of mortalin potentiates amyloid-␤-mediated mitochondrial dysfunction and cytotoxicity. Conclusion: Inhibition of mortalin could lead to mitochondrial dysfunction through mitochondrial fragmentation. Significance: Activation of mortalin may antagonize the progression of A␤-mediated neuronal injury in which mitochondrial dysfunction has a key role.

BackgroundAutophagy has paradoxical and complex functions in cancer development, and autophagy-related genes (ATG) are key regulators in autophagy. Until now, more than 30 different ATG proteins have been identified in yeast, and their mammalian counterparts also have been reported. Although the roles of a few ATG proteins in cancer have been characterized, the role of ATG10 is almost completely unknown.Methodology/Principal FindingsTo investigate the clinicopathological role of ATG10 in colorectal cancer, we analyzed ATG10 expression in colorectal cancer tissues and cell lines. Protein expression analysis showed that ATG10 is highly increased in colorectal cancer (tissue - 18/37 cases, 48%; cell line –8/12 cell lines, 66%). Immunohistochemical analysis with clinicopathological features indicated a strong association of the up-regulation of ATG10 with tumor lymph node metastasis (p = 0.005) and invasion (p<0.001). Moreover, both 5-year disease free survival and overall survival rates of patients bearing tumors that did not express ATG10 were significantly higher than those of patients bearing ATG10-expressing tumors (p = 0.012).Conclusion/SignificanceIncreased expression of ATG10 in colorectal cancer is associated with lymphovascular invasion and lymph node metastasis indicating that ATG10 may be a potential prognostic maker in colorectal cancer.