miR126-Mediated Signal Transducer and Activator of Transcription 3 Signaling Pathway Regulates the Malignant Biological Behavior of Pancreatic Cancer Cells

Abstract

Background and purpose: As a type of non-coding genetic material widely existing in eukaryotes, a growing amount of research have confirmed that it have close connection with the occurrence and progression of various malignancies. MicroRNA126 is increased in non-small-cell lung cancer, liver cancer and gastric carcinoma. The up-regulation of miR126 in cervical cancer is closely associated with the clinical staging, histological grade, depth of invasion and early metastasis of the tumor, and it is also of great value in predicting the survival prognosis of the tumor. However, there is little known about the relationship between miR126 and pancreatic carcinoma. Therefore, this study explored the miR126-mediated STAT3 signaling pathway in medicating pancreatic cancer cell multiplication, migration, cell cycle and apoptosis in vitro . Methods: PANC-1 cell (human pancreatic cancer cell line) was selected for routine resuscitation and subculture. The experiment is grouped as: blank control group (NC group), empty plasmid transfection group (miR126-NC group), miR126mimic transfection group (overexpression Group) and miR126 inhibition plasmid transfection group (low expression group); cell viability of each group for 12 h, 24 h, 48 h and 72 h was detected using MTT assay. Wound healing assay was used to evaluated the ability of cell migration. Flow cytometry was performed to analyze cell cycle. The mRNA expression of Caspase-3 was determined by reverse transcription PCR (RT-PCR). STAT3 protein was evaluated by western blot. Results: miR126 overexpression significantly increased cell proliferation at 12 h, 24 h, 48 h, and 72 h, while the cell proliferation rates of the low expression group at each time point were significantly reduced in comparision with those of the NC group and the miR126-NC group (P < 0 05). miR126 overexpression significantly induced cell migration, while miR126 low-expression significantly inhibited cell migration (P < 0 05). miR126 overexpression significantly enhanced the percentage of G2/M, while the percentage of G2/M in the low-expressed group was remarkably reduced in comparision with those of the NC group and the miR126-NC group (P < 0 05). The mRNA expression of Caspase-3 was significantly inhibited in miR126 overexpression group, while the expression of Caspase-3 mRNA in the cells with miR126 low expression was remarkably increased (P < 0 05). The protein expression of STAT3 in miR126 overexpression group was notably up-regulated, while the expression level of STAT3 protein in the low expression group was prominently down-regulated (P <0 05). Conclusion: MiR126 overexpression may induces the STAT3 signaling pathway and then regulates cell proliferation, cell migration, cell cycle arrest and cell apoptosis in pancreatic carcinoma.