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Noncoding RNAs as key modulators of autophagy in pancreatic cancer (Review).

Inability of early detection as well as lack of proper therapeutic intervention, both add to the complexity of pancreatic cancer. Understanding of the basic cellular processes is of the utmost importance and autophagy is one of these processes. Considering the importance of this process in normal cellular functions as well as in pathological states, elaboration of the updated information on the mechanism of autophagy was initially carried out. Autophagy is a process for degradation of damaged cellular organelles, abnormal proteins and even nutrients which happen via formation of autophagosomes. Incidentally, autophagy has been shown to play both oncogenic and tumour‑suppressive functions in cancer and has also been shown to modulate stemness of cancer cells, recurrence and resistance to chemotherapeutic agents. The contribution of autophagy genes and pathways in pancreatic tumorigenesis was also evaluated. Regulation is the key step in any such cellular phenomenon and noncoding RNA‑mediated regulation is an emerging field. While miRNAs participate mainly in post‑transcriptional regulation, long noncoding RNAs and circular RNAs have more diverse regulatory functions. Noncoding RNAs are also shown to modulate both the tumour‑promoting and tumour‑suppressing functions of autophagy in pancreatic cancer. The implication of noncoding RNA‑mediated regulation with respect to radio‑resistance and chemo‑resistance of pancreatic cancer cells was also assessed. To the best of our knowledge, this is the first ever attempt trying to decipher the cross‑talk between autophagy‑noncoding RNAs and genes involved in the development and progression of pancreatic cancer.