Abstract

Extracellular vesicles, specifically exosomes, play a significant role as an extracellular messenger through their transporting cargo. Of particular interest are the potential roles they play in pancreatic cancer, one of the leading causes of cancer-related mortality worldwide. Pancreatic Ductal Adenocarcinoma displays high chemo-resistance and metastatic ability, which may be influenced by cancer-derived exosomes carrying proteins, lipids and RNA. To date, among the most extensively examined exosomal molecular cargo there are long non-coding RNAs (lncRNAs) that, despite the increasing interest in their role and functions, are relatively poorly understood compared to other RNA transcripts. Nevertheless, we have witnessed an increasing interest for lncRNAs roles and functions in the past decade. For example, lncRNAs have been investigated as potential biomarkers for diagnosing pancreatic cancer and may have a role as therapeutics targets for precision medicine, but may also directly intervene in tumour progression features such as metastasis, epithelial to mesenchymal transition and resistance of cancer cells towards chemotherapy agents. The function of lncRNAs within various cancer exosomes is still undefined. In this review, we summarize the current knowledge on pancreatic cancer-derived exosome specific lncRNAs having prominent roles in genome integrity, pancreatic cancer progression and in other oncogenic hallmarks.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.