Published online Apr 21, 2020. doi: 10.3748/wjg.v26.i15.1745
Peer-review started: December 16, 2019
First decision: January 19, 2020
Revised: February 7, 2020
Accepted: March 19, 2020
Article in press: March 19, 2020
Published online: April 21, 2020
Processing time: 127 Days and 2.6 Hours
The incidence and mortality rates of pancreatic carcinoma (PC) are rapidly increasing worldwide. Long noncoding RNAs (lncRNAs) play critical roles during PC initiation and progression. Since the lncRNA DNAH17-AS1 is highly expressed in PC, the regulation of DNAH17-AS1 in PC was investigated in this study.
To investigate the expression and molecular action of lncRNA DNAH17-AS1 in PC cells.
The PC expression data for the lncRNA DNAH17-AS1 was downloaded from The Cancer Genome Atlas database and used to examine its profile. Western blot and reverse transcription-quantitative PCR were employed to assess protein and mRNA expression. A subcellular fractionation assay was used to determine the location of DNAH17-AS1 in cells. In addition, the regulatory effects of DNAH17-AS1 on miR-432-5p, PPME1, and tumor activity were investigated using luciferase reporter assay, MTT viability analysis, flow cytometry, and transwell migration analysis.
DNAH17-AS1 was upregulated in PC cells and was associated with aggressive tumor behavior and poor prognosis for patients. Silencing DNAH17-AS1 promoted the apoptosis and reduced the viability, invasion, and migration of PC cells. In addition, DNAH17-AS1 served as a PC oncogene by downregulating miR-432-5p which normally directly targeted PPME1 to downregulate its expression.
DNAH17-AS1 functions in PC as a tumor promoter by regulating the miR-432-5p/PPME1 axis. This finding may provide new insights for PC prognosis and therapy.
Core tip: DNAH17-AS1 is upregulated in pancreatic carcinoma (PC) and is associated with aggressive clinical presentation in PC patients. DNAH17-AS1 promotes PC cell viability, invasion, and migration, and its silencing promotes PC cell apoptosis. DNAH17-AS1 is found primarily in the cytoplasm and participates in the competing endogenous RNA regulatory network. DNAH17-AS1 functions as a tumor promoter in PC by downregulating miR-432-5p and upregulating PPME1.