Role of Non-Coding RNAs in Pancreatic Ductal Adenocarcinoma Associated Cachexia

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American journal of physiology. Cell physiology


Cachexia is an acute syndrome that is very commonly observed in patients with cancer. Cachexia is the number one cause of death in patients with metastatic disease and is also the major factor for physical toxicity and financial burden. More importantly, the majority of advanced stage pancreatic ductal adenocarcinoma (PDAC) cancer patients undergo cachexia. Pancreatic cancer causes deaths of 50,000 Americans and about 400,000 people worldwide every year. The high mortality rates in metastatic PDAC is due to systemic pathologies and cachexia which quickens death in these patients. About 90% of all PDAC patients undergo wasting of muscle causing mobility loss leading to a number of additional pathological conditions. PDAC associated cancer cachexia emanates from complex signaling cues involving both mechanical and biological signals. Tumor invasion associated with the loss of pancreatic function induced digestive disorders, malabsorption which causes subsequent weight loss and eventually promotes cachexia. Besides, systemic inflammation of PDAC patients could release chemical cues (e.g. cytokine mediated Atrogin-1 and MAFbx expression) that participate in muscle wasting. Our understanding of genes, proteins and cytokines involved in promoting cancer cachexia has evolved considerably. However, the role of epigenetic factors, particularly the role of non-coding RNAs (ncRNAs) in regulating PDAC associated cachexia is less studied. In this review article, the most updated knowledge on the various ncRNAs including microRNAs (miRs), long non-coding RNA (lncRNAs), piwi interacting RNAs (PiwiRNAs), snoRNAs and circular RNAs (circRNA) and their roles in cancer cachexia are described.

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ePub ahead of print