Abstract

Considering the significance of LINC01061 in papillary thyroid cancer, here, we commenced to study the role of LINC01061 in autoimmune thyroid disease (AITD) and the potential mechanism. Thyroid tissues were attained from patients with AITD, and Nthy-ori 3–1 cells were induced with lipopolysaccharide (LPS), followed by measurement of LINC01061, microRNA (miR)-612, and BRD4 expression as well as their binding relation. The ectopic expression and silencing experimentations were carried out in LPS-induced Nthy-ori 3–1 cells to detect cell viability and apoptosis as well as inflammation and inflammasome. BRD4 and LINC01061 upregulation and miR-612 downregulation were observed in thyroid tissues of AITD patients and LPS-induced Nthy-ori 3–1 cells. Mechanistic analysis manifested that LINC01061 bound to miR-612 that negatively targeted BRD4. LINC01061 upregulated BRD4 to enhance cell viability, trigger inflammation and inflammasome activation but reduce apoptosis of LPS-induced Nthy-ori 3–1 cells by sponging miR-612. In conclusion, LINC01061 induced the occurrence of AITD by upregulation of miR-612-mediated BRD4 expression.