IncRNA XIST Stimulates Papillary Thyroid Cancer Development through the miR-330-3p/PDE5A Axis.

Long non-coding RNAs (lncRNAs) possess both tumor suppressive and oncogenic functions in papillary thyroid cancer (PTC). Among all the thyroid cancers, PTC is the most prevalent form. Herein, we aim to determine the regulatory mechanisms and functions of lncRNA XIST in the multiplication, invasion, and survival of PTC. Quantitative reverse transcription polymerase chain reaction and Western blot experiments were performed to determine the patterns of lncRNA XIST, miR-330-3p, and PDE5A expressions. The subcellular localization of XIST was determined through subcellular fractionation. Bioinformatics analyses were performed to determine miR-330-3p's relationships with XIST and PDE5A, which were further confirmed through luciferase reporter assays. Loss-of-function combined with Transwell, CCK-8, and caspase-3 activity experiments were performed to determine the mechanism of the XIST/miR-330-3p/PDE5A axis in regulating the malignancy of PTC cells. Xenograft tumor experiment was employed to study the influence of XIST on tumor development in vivo. The PTC cell lines and tissues manifested considerably high levels of lncRNA XIST expression. The XIST knockdown inhibited proliferation, blocked migration, and strengthened apoptosis among PTC cells. Moreover, its knockdown suppressed PTC tumor development in vivo. XIST repressed miR-330-3p to stimulate the malignant behaviors of PTC. Through the downregulation of PDE5A, miR-330-3p attenuated the capability of PTC cells to grow, migrate, and survive. lncRNA XIST promotes tumor development in PTC through the regulation of the miR-330-3p/PDE5A axis. The findings from this study provide new insights into the treatment of PTC.

Long noncoding RNA BBOX1-AS1 promotes the progression of gastric cancer by regulating the miR-361-3p/Mucin 13 signaling axis.

Gastric cancer (GC) places a heavy burden on global health, and the information on the molecular mechanism of the progression of GC is still inadequate. Long noncoding RNA (LncRNA) has been confirmed to be widely involved in regulating the progression of GC. Our aim in this study was to explore the role and potential regulatory mechanism of lncRNA BBOX1-AS1 in GC. The expression levels of BBOX1-AS1, miR-361-3p, and MUC13 in GC tissues and cells were evaluated using quantitative real-time polymerase chain reaction and western blotting. The silencer of BBOX1 antisense RNA 1 (BBOX1-AS1) and mucin 13 (MUC13), the mimics and inhibitor of miR-361-3p, and their negative controls were used to alter the expression of these genes. Luciferase reporter, pull-down, and RNA immunoprecipitation assays were performed to verify the correlation between miR-361-3p, BBOX1-AS1, and MUC13. GC cell proliferation, invasion, and apoptosis were detected by cell counting kit-8, transwell, and flow cytometry assays, respectively. An in vivo functional experiment was performed to assess the effect of BBOX1-AS1 on GC. The results showed that BBOX1-AS1 was significantly upregulated in GC tissues. Silencing of BBOX1-AS1 inhibited GC cell proliferation and invasion and inhibited tumor growth in vivo, whereas it promoted apoptosis. MiR-361-3p was significantly downregulated in GC and counteracted the inhibitory effects of BBOX1-AS1 on GC progression. MUC13, which is targeted by miR-361-3p, is significantly upregulated in GC. MUC13 silencing inhibited GC progression was aborgated by miR-361-3p inhibitor. Collectively, BBOX1-AS1 silencing inhibits GC progression by regulating the miR-361-3p/MUC13 axis, providing a potential therapeutic biomarker for GC.