Long non-coding RNA LINC01004 promotes malignant behaviors of pituitary adenoma via miR-323a-3p/136-5p/RCN2 axis.

Pituitary adenoma (PA) is a common intracranial tumor, and its incidence has been on the rise in recent years. Pituitary tumor not only causes intracranial space occupying signs, but also produces endocrine disorders, such as infertility, sexual dysfunction, facial and limb changes. Moreover, it destroys the internal environment stability and even affects the appearance of a person. However, the mechanism of PA is not fully understood. Previous research has confirmed that the expression or role of long non-coding RNA is closely connected with the occurrence of human diseases. In this study, we discovered that long intergenic non-protein coding RNA 1004 (LINC01004) was aberrantly up-regulated in PA cells. Functional assays manifested that LINC01004 promoted malignant behaviors of PA cells in vitro and growth of PA in vivo. By using bioinformatics tools and a series of mechanism assays, LINC01004 was identified to sponge miR-323a-3p/miR-136-5p to enhance the expression of RCN2 in PA. In conclusion, the results provided in this study revealed a novel regulatory mechanism of LINC01004 in PA, which might be helpful for the treatment of PA and supply a new thought for further research of PA.

Long Noncoding RNA PSMA3 Antisense RNA 1 Promotes Cell Proliferation, Migration, and Invasion in Pancreatic Ductal Adenocarcinoma Via Targeting MicroRNA-154-5p to Positively Modulate Karyopherin Subunit Alpha 4.

OBJECTIVES: Pancreatic ductal adenocarcinoma (PDAC), as the most frequent pancreatic tumor, featuring high death rate. The current study intends to explore the biological role of PSMA3 antisense RNA 1 (PSMA3-AS1) and its mechanism underlying PDAC progression. METHODS: Expression analyses were conducted using quantitative reverse transcription-polymerase chain reaction. Proliferative, apoptotic, migratory, and invasive capacities were determined by functional assays, encompassing 5-ethynyl-2'-deoxyuridine, colony formation, JC-1, terminal deoxynucleotidyl transferase dUTP nick-end labeling, and transwell assays in PDAC cells. The RNA-binding protein immunoprecipitation, RNA pulldown, and luciferase reporter assays uncovered the biological and regulatory role of PSMA3-AS1 in PDAC. RESULTS: Long noncoding RNA PSMA3-AS1 was aberrantly overexpressed in PDAC cells. Downregulated PSMA3-AS1 repressed cell proliferative, migratory, and invasive capacities and propelled cell apoptosis of PDAC. MicroRNA-154-5p (miR-154-5p) was proved to be targeted by PSMA3-AS1 in PDAC cells. Karyopherin subunit alpha 4 (KPNA4) was the downstream target messenger RNA of miR-154-5p. Karyopherin subunit alpha 4 knockdown hindered cell proliferation, migration, and invasion in PDAC. In rescue assays, KPNA4 overexpression or miR-154-5p interference counteracted the inhibitory influence of PSMA3-AS1 ablation on the progression of PDAC cells. CONCLUSIONS: Our results suggested that PSMA3-AS1 enhances PDAC cell proliferative, migratory, and invasive capacities via modulating miR-154-5p/KPNA4 axis.