Abstract

Emerging evidence has demonstrated that miR-223 is critically involved in the progression of pancreatic cancer (PC); however, the underlying mechanisms are not fully elucidated. In the present study, we explored the molecular basis of miR-223-mediated tumor progression in PC. We performed numerous approaches including MTT, FACS, transfection, RT-PCR, western blotting, Transwell, and animal studies to determine the physiological role of miR-223 in PC cells. We found that sister chromatid cohesion protein PDS5 homolog B (PDS5B) is a direct target of miR-223 in PC. Moreover, PDS5B exhibits tumor-suppressive function in PC cells. Consistently, ectopic overexpression of PDS5B reversed miR-223-mediated tumor progression in PC cells. These results suggest that the miR-223/PDS5B axis regulates cell proliferation and invasion in PC cells. Our findings indicated that downregulation of miR-223 could be a novel therapeutic approach for PC.

Highlights

  • Pancreatic cancer (PC) patients often have high morbidity and mortality

  • Overexpression of miR-223 Promotes Cell Growth and Inhibits Cell Apoptosis in pancreatic cancer (PC) Cells To explore the role of miR-223 in PC cell growth, an MTT assay was performed in PC cells after miR-223 mimic or miR-223 inhibitor treatments

  • Cell apoptosis assays revealed that overexpression of miR-223 suppressed cell apoptosis in PC cells

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Summary

Introduction

PC could lead to 44,330 deaths in the United States in 2018.1 It is expected that there will be 55,440 new cases of PC in the United States this year.[1] In contrast to the steady increase in survival of most cancer types, the 5-year survival rate is 8% for PC patients, as these patients are typically diagnosed at a distant stage.[1,2] Another reason for the relatively low survival rate of PC is because of intrinsic and extrinsic drug resistance to chemotherapy.[3,4] Without a doubt, it is pivotal to explore the molecular mechanism of PC development and progression and develop a novel therapeutic strategy for the treatment of PC. The role of miR-223 is investigated in PC, the molecular mechanism of miR-223-induced tumor progression is largely elusive

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