MiR-155 regulates the proliferation and apoptosis of pancreatic cancer cells through targeting SOCS3.

Abstract:

OBJECTIVE:Reduced expression of suppressors of cytokine signaling 3 (SOCS3) is associated with a variety of tumors. The elevated miR-155 expression is associated with the onset of pancreatic cancer. Bioinformatics analysis revealed a targeted relation between miR-155 and the 3'-UTR of SOCS3. This study investigated whether miR-155 regulates SOCS3 expression and affects the biological effects of pancreatic cancer cells. PATIENTS AND METHODS:QRT-PCR was used to detect the expression of miR-155 and SCOS3 mRNA in tumor tissues and paracancerous tissues of patients with pancreatic cancer. The dual luciferase reporter gene assay validated the target interaction between miR-155 and SOCS3. Pancreatic cancer cell line SW1990 cells were divided into miR-NC group and miR-155 inhibitor group followed by an analysis of the expressions of SOCS3, p-JAK2 and p-STAT3, cell apoptosis by flow cytometry, and cell proliferation by EdU staining. RESULTS:Compared with adjacent tissues, miR-155 expression was increased in tumor tissues of patients with pancreatic cancer, and SOCS3 expression was decreased. There was a targeted regulatory relationship between miR-155 and SOCS3 mRNA. Compared with HPDE6-C7 cells, miR-155 expression in pancreatic cancer SW1990 and Capan-1 cells was increased, and SOCS3 expression was decreased. Transfection of miR-155 inhibitor significantly increased SOCS3 expression in pancreatic cancer SW1990 cells, decreased the expression of p-JAK2 and p-STAT3, increased cell apoptosis, and decreased cell proliferation. CONCLUSIONS:Increased miR-155 expression and decreased SOCS3 expression are related to the pathogenesis of pancreatic cancer. miR-155 inhibits the proliferation and apoptosis of pancreatic cancer cells by inhibition of SOCS3 expression.

authors

Wang J,Guo J,Fan H

doi

10.26355/eurrev_201906_18181

subject

Has Abstract

pub_date

2019-06-01 00:00:00

pages

5168-5175

issue

12

eissn

1128-3602

issn

2284-0729

journal_volume

23

pub_type

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