Thyroid cancer (TC) remains a prevalent public health concern. To further study the molecular mechanism of TC development, we explored the regulatory mechanism and function of lncRNA ARAP1-AS1 in TC progression.
The verification of ARAP1-AS1, PDE5A and miR-516b-5p expression levels among the TC cell lines and tissues was fulfilled via RT-qPCR and western blot analyses. Cell Counting Kit-8 and colony formation experiments were executed to assess ARAP1-AS1’s biological function in vitro. Western blotting was conducted to assess apoptosis through the expressions of apoptotic markers. A tumor xenograft experiment was conducted to evaluate whether ARAP1-AS1 affected TC tumor development in vivo. The interactions of miR-516b-5p with ARAP1-AS1 and PDE5A were explored through a dual-luciferase reporter and RNA Binding Protein Immunoprecipitation assays, as well as through Pearson’s correlation analysis.
ARAP1-AS1 and PDE5A were evidently upregulated in the TC cell lines and tissues whereas miR-516b-5p was poorly expressed. ARAP1-AS1 silencing in TC cells hampered cell proliferation, reduced their viability and boosted apoptosis. Moreover, it inhibited tumor growth in vivo. ARAP1-AS1 had been revealed to be correlated negatively to miR-516b-5p. Finally, we demonstrated that the miR-516b-5p inhibitor was capable of reversing ARAP1-AS1-knockdown’s repressive effects on TC cell development by means of regulating PDE5A expression.
ARAP1-AS1 partially facilitated TC cell development and survival through the modulation of miR-516b-5p/PDE5A axis. This contributes a novel biomarker and new perspectives for TC treatment.