Abstract
BackgroundThe prognosis of pancreatic cancer (PC) is relatively dismal due to the lack of effective therapy. In this study, we explored the specific functions and molecular mechanisms of miR-107 to uncover effective therapeutic targets for PC.MethodThe miR-107 expression in PC cell lines was assessed via quantitative real-time polymerase chain reaction (qRT-PCR). Besides, online bioinformatics analysis was adopted to predict the underlying targets of miR-107. Meanwhile, TCGA database was employed to explore the prognosis of PC patients. In addition, MTT and transwell assays were conducted to explore the PC cells’ biological functions.ResultMiR-107 was remarkably increased in PC cells which could promote the proliferation, invasion and migration of PC cells. In addition, miR-107 could directly down-regulate TGFBR3 expression through binding to TGFBR3 3’UTR. Survival analysis from TCGA suggested that PC patients with higher miR-107 expression was significantly involved in poorer prognosis.ConclusionWe concluded that miR-107 promoted proliferation, invasion and migration of PC cells via targeting TGFBR3, which may provide novel underlying therapeutic targets.
Highlights
pancreatic cancer (PC) is the third leading cause of cancer-correlated deaths in the United States [1]
We concluded that miR-107 promoted proliferation, invasion and migration of PC cells via targeting TGFBR3, which may provide novel underlying therapeutic targets
MiRNA-107 enhances the malignant progression of pancreatic cancer
Summary
PC is the third leading cause of cancer-correlated deaths in the United States [1]. Most PC patients were diagnosed at advanced stages due to rare early diagnosis of PC. It is required to uncover potential molecular mechanisms and valuable therapeutic targets. Zhao et al suggested that miRNA-221-3p desensitized PC cells to 5-fluorouracil via targeting RB1 [6]. Zhao et al found that miRNA-141, downregulated in pancreatic cancer, inhibited cell proliferation and invasion through directly targeting MAP4K4 [7]. A recent report suggested that miR-107 was overexpressed in gastric cancer cells [10]. In this present paper, we uncovered that miR-107 was upregulated in PC on the basis of high-throughput data. We explored the specific functions and molecular mechanisms of miR-107 to uncover effective therapeutic targets for PC. Editor: Suhwan Chang, University of Ulsan College of Medicine, REPUBLIC OF KOREA
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