Long noncoding RNA LINC00184 facilitates the proliferation, metastasis, and adenine metabolism of cholangiocarcinoma via modulating hsa-miR-23b-3p/ANXA2 axis.

ABSTRACT

The purpose of this article was to probe the mechanism underlying long noncoding RNA (lncRNA)-LINC00184 in cholangiocarcinoma development and to investigate the effects of LINC00184 on cholangiocarcinoma. We used bioinformatics to analyze the expression of LINC00184, microRNA (miR)-23b-3p and ANXA2 in cholangiocarcinoma tissues. The levels of LINC00184, miR-23b-3p, and ANXA2 were detected by qRT-PCR. Cell proliferation was tested by CCK8. Transwell assay was used to detect cell invasion and migration. The target connection between LINC00184, miR-23b-3p, or ANXA2 was probed by luciferase reporter assay. RNA pull-down method was employed to test the relationship among LINC00184/miR-23b-3p/ANXA2 in cholangiocarcinoma cells. The Pearson correlation coefficient analyzed was applied to analyze the correlation among LINC00184, miR-23b-3p, and ANXA2. LC-MS/M analysis was used to explore whether the changes of adenine metabolism was affected by LINC00184 in cholangiocarcinoma cells. We discovered that LINC00184 expression was heightened in cholangiocarcinoma patients and cells. Knockdown of LINC00184 repressed cell proliferation, invasion, migration and adenine metabolism in cholangiocarcinoma cells. miR-23b-3p was regarded as a target of LINC00184 and its depletion perversed the inhibitive influence of LINC00184 silencing on cholangiocarcinoma cells. ANXA2 was a target of miR-23b-3p and was negatively modulated by miR-23b-3p. Moreover, ANXA2 was positively modulated by LINC00184 via sponging miR-23b-3p. In short, silencing of LINC00184 suppressed cell proliferation, invasion and migration through over-expression of miR-23b-3p and reducing of ANXA2 in cholangiocarcinoma cells. These findings contribute to understanding the influences of LINC00184, miR-23b-3p, and ANXA2 on cholangiocarcinoma and provide basis for cholangiocarcinoma treatment.