Autophagy-Related Gene Expression Changes Are Found in Pancreatic Cancer and Neurodegenerative Diseases

Abstract

Genetic alterations can cause cancer, including pancreatic cancer (PC) as well as certain neurodegenerative diseases. Our lab has recently identified genes that are modulated during pancreatic cancer liver metastasis, and some are known to have a role in neurobiology or neurodegenerative diseases. Autophagy or self-eating portrays the lysosomaldependent degradation and recycling of protein aggregates and defective organisms in eukaryotic cells. Deregulation of autophagy as a cellular mechanism is common in neurodegenerative diseases as well as cancer and may represent a platform by which some genes can affect both disorders. This is exemplified for optineurin, which is an autophagy receptor that was found among genes with intensive modulation of expression in PC liver metastasis. Our results on this autophagy receptor draw the attention to the expression status of this and other autophagy genes in pancreatic cancer progression.

Adding Some “Splice” to Stress Eating: Autophagy, ESCRT and Alternative Splicing Orchestrate the Cellular Stress Response

“…The activation of autophagy is initiated by the protein kinase AMPK in response to the cellular stresses as mentioned above. In addition, the cellular response to these same stresses also involves changes to the transcriptional landscape [63,64]. These transcriptional changes have been associated with altered mRNA splicing, which results in alternative splicing of genes that regulate autophagosome formation.…”