Open AccessmiR‑31 promotes tumorigenesis in ulcerative colitis‑associated neoplasia via downregulation of SATB2
Author(s) -
Yan Song,
Kui Jiang,
Bangmao Wang,
WenTian Liu,
Rui Lin
Publication year - 2020
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2020.11573
Subject(s) - carcinogenesis , oncogene , microrna , ulcerative colitis , biology , downregulation and upregulation , gene , dysplasia , molecular medicine , gene expression , pathogenesis , cancer research , cell cycle , immunology , genetics , disease , medicine , pathology
Ulcerative colitis (UC) features chronic, non-infectious inflammation of the colon. The risk of ulcerative colitis‑associated neoplasia (UCAN) increases in direct association with the duration of this disease. Whether miRNAs exert a regulatory effect on the pathogenesis of UCAN has remained to be elucidated. In the present study, differentially expressed genes (DEGs) and microRNAs (miRNAs/miRs) were identified using bioinformatics analysis of Gene Expression Omnibus datasets. Enrichment analyses were performed to determine the function of the DEGs. The target genes of key miRNAs were predicted using miRWalk. Validation of DEGs and miRNAs in patients with UC, UC with low‑grade dysplasia and UC with high‑grade dysplasia (UC‑HGD) was performed using reverse transcription‑quantitative PCR analysis. A total of 38 differentially expressed miRNAs and 307 mRNAs were identified from the profiles and miR‑31 was validated as being overexpressed in UCAN tissues, particularly in the UC‑HGD samples. Furthermore, special AT‑rich DNA‑binding protein 2 (SATB2) was validated as a target gene of miR‑31 and SATB2 expression was negatively correlated with miR‑31 expression. Therefore, miR‑31 is upregulated in UCAN and it may promote tumorigenesis through downregulation of SATB2.