MiR-216b inhibits pancreatic cancer cell progression and promotes apoptosis by down-regulating KRAS
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Submission date: 2017-09-12
Final revision date: 2017-10-10
Acceptance date: 2017-10-18
Online publication date: 2017-12-31
Publication date: 2018-10-31
Arch Med Sci 2018;14(6):1321-1332
Pancreatic cancer is a highly lethal malignancy with high invasion metastasis, which is difficult to diagnose and treat. MicroRNA-216b (miR-216b) plays an important role in many types of tumors. In this study, we explore how miR-216b affected human pancreatic cancer cell development by targeting KRAS.

Material and methods:
Expression level of miR-216b and KRAS in tissue samples and cells were detected by RT-PCR and western blot. Immunohistochemical assay analysed the expressions of KRAS protein in tumor and adjacent tissues. The target relationship between miR-216b and KRAS was validated by dual-luciferase reporter assay. Pancreatic cancer cell proliferation, migration, invasion and apoptosis abilities of cells transfected with miR-216b mimics and KRAS-siRNA, Panc-1 were detected by MTT assay, transwell assay and flow cytometry assay respectively. Prognosis of patients with different expression levels of miR-216b and KRAS were analyzed by Kaplan-Meier survival analysis and Cox proportional hazards regression model.

The expression of miR-216b in pancreatic cancer tissue and cell line was down-regulated (p < 0.01), while KRAS expression was up-regulated (p < 0.01) compared with adjacent normal tissues. Both the expressions of miR-216b and KRAS have a strong influence on prognosis of the pancreatic cancer patients (p = 0.024 and p = 0.017). The dual-luciferase reporter assay verified that miR-216b directly targeted KRAS in pancreatic cancer cells. Overexpression of miR-216b reduced the expression of mRNA and protein of KRAS (p = 0.013 and p = 0.003), but silencing KRAS had no effect on miR-216b expression (p = 0.706). By silencing KRAS or up-regulation of miR-216b could suppress cell proliferation, migration and invasion of pancreatic cancer cells and promote apoptosis.

MiR-216b might inhibit pancreatic cancer cell progression and stimulate apoptosis by silencing KRAS.

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