MiR-489-3p modulates cell proliferation and apoptosis in cerulein-induced acute pancreatitis by targeting X-linked inhibitor of apoptosis protein
Xiang Li 1,2
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1
Critical Care Unit, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, P.R. China
2
Emergency Department (one) of Hunan Provincial People’s Hospital, Changsha, Hunan, P.R. China
3
Xiangya School of Public Health, Central South University, Changsha, Hunan, P.R. China
4
Emergency Department (three) of Hunan Provincial People’s Hospital, Changsha, Hunan, P.R. China
CORRESPONDING AUTHOR
Zhanhong Tang   

Critical Care Unit, The First Affiliated Hospital of Guangxi Medical University
Submission date: 2019-08-15
Final revision date: 2020-01-16
Acceptance date: 2020-02-02
Online publication date: 2021-03-16
 
 
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ABSTRACT
Introduction:
This study aims to explore the effect and mechanism of miR489-3p on the proliferation and apoptosis of pancreatic acinar cells in acute pancreatitis (AP).

Material and methods:
X-linked inhibitor of apoptosis protein (XIAP) and miR-489-3p expression in serum of AP patients, pancreatic AR42J cells, and rat AP tissues were measured using quantitative reverse transcription polymerase chain reaction and western blot. The effect of miR-489-3p on proliferation and apoptosis was determined by MTT assay and flow cytometry. The relationship between XIAP and miR-489-3p was verified using luciferase assay RNA immunoprecipitation assay. Histological changes in rat pancreatic tissues were observed via haematoxylin and eosin staining.

Results:
Measurement of miR-489-3p and XIAP expressions in AP patients revealed a negative correlation between miR-489-3p and XIAP. Increased miR-489-3p expression in AP patients indicated a poor prognosis. Cerulein was used to induce AP in AR42J cells and standard deviation rats. Experiments in cells and AP rat models showed that miR-489-3p can increase cell apoptosis and inhibit cell proliferation by regulating XIAP, as shown by elevated expressions of pro-apoptotic proteins (p53 and Bax) and decreased expression of proliferation indicator (Ki-67) after transfection of miR-489- 3p mimics. Meanwhile, knockdown of miR-489-3p abrogated the inhibitory effects of miR-489-3p on cell proliferation and the promotion on cell apoptosis. Luciferase assay and RNA immunoprecipitation assay confirmed that XIAP can directly bind miR-489-3p.

Conclusions:
We concluded that miR-489-3p modulates cell proliferation and apoptosis in AP by targeting XIAP. Given that high expression of miR489-3p in AP indicated poor prognosis, it raises the possibility that miR489-3p might be a novel and valuable therapeutic target and a prognosis indicator for AP.

eISSN:1896-9151
ISSN:1734-1922