Abstract
Anaplastic thyroid cancer (ATC) is the most common malignant endocrine tumors which resist to majority treatment. Thus, there is impelling need to figure out the mechanism of progress of ATC. In this study, we explored the function and mechanism of lncRNA actin filamentin-1 antisense RNA (AFAP-AS1) which provided a new biomarker for ATC. Viabilities and apoptosis were tested by CCK-8, colony formation and flow cytometry. The interactions between miR-155-5p and AFAP-AS1 or ETS1 was detected by luciferase reporter assays. ETS proto-oncogene1/mitogen-activated protein kinase1 (ETS1/ERK) pathway was assessed by Western blot. Xenograft models were built to confirm the function of AFAP-AS1 in vivo. Firstly, we showed that relative RNA expression of AFAP-AS1 in ATC cells was higher than in immortalized thyroid cells. Next, AFAP-AS1 was verified as an oncogene in ATC since knock-down of AFAP-AS1 inhibited cell proliferation and accelerated apoptosis. In addition, miR-155-5p was negatively regulated by AFAP-AS1. Moreover, AFAP-AS1 regulated ETS1/ERK pathway by sponging miR-155-5p. Finally, we confirmed knock-down of AFAP-AS1 significantly suppressed tumor proliferation in vivo. Our research proved that AFAP-AS1 could facilitate progression of thyroid cancer sponging miR-155-5p through ETS1/ERK pathway.