Investigating the regulatory role of miRNAs as silent conductors in the management of pathogenesis and therapeutic resistance of pancreatic cancer.

Pancreatic cancer (PC) has the greatest mortality rate of all the main malignancies. Its advanced stage and poor prognosis place it at the bottom of all cancer sites. Hence, emerging biomarkers can enable precision medicine where PC therapy is tailored to each patient. This highlights the need for new, highly sensitive and specific biomarkers for early PC diagnosis. Prognostic indicators are also required to stratify PC patients. To avoid ineffective treatment, adverse events, and expenses, biomarkers are also required for patient monitoring and identifying responders to treatment. There is substantial evidence that microRNAs (miRs, miRNAs) play a critical role in regulating mRNA and, as a consequence, protein expression in normal and malignant tissues. Deregulated miRNA profiling in PC can help with diagnosis, treatment planning, and prognosis. Furthermore, knowledge of the primary effector genes and downstream pathways in PC can help pinpoint potential miRNAs for use in treatment. Different miRNA expression profiles may serve as diagnostic, prognostic markers, and therapeutic targets across the spectrum of malignant pancreatic illness. Dysregulation of miRNAs has been linked to the malignant pathophysiology of PC through affecting many cellular functions such as increasing invasive and proliferative prospect, supporting angiogenesis, cell cycle aberrance, apoptosis elusion, metastasis promotion, and low sensitivity to particular treatments. Accordingly, in the current review, we summarize the recent advances in the roles of oncogenic and tumor suppressor (TS) miRNAs in PC and discuss their potential as worthy diagnostic and prognostic biomarkers for PC, as well as their significance in PC pathogenesis and anticancer drug resistance.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors have declared that no competing interests exist.
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