LncRNA ROR promotes proliferation, immune escape, and polarization of M2 macrophages in thyroid cancer by activating the PI3K/AKT pathway.

Abstract

Thyroid cancer is the most prominent type of endocrine cancer. LncRNA ROR (Linc- ROR) exerts tumor regulator function in cancers. This study elucidates the action of Linc-ROR on thyroid cancer. The Linc-ROR level were investigated in 70 thyroid cancer patients. Cell viability was detected utilizing CCK-8 method. The xenograft tumor was constructed to evaluate tumor growth. The proportion of CD8+ T cells was assessed using flow cytometry. IL-10, IFN-γ, and TNF-β levels were detected utilizing ELISA assays. The Linc-ROR level was elevated in thyroid cancer patients (n = 70). The up-regulated Linc-ROR was associated with poor overall survival (p = 0.0315), lymph node metastasis (p = 0.027), and TNM stage (p = 0.016). Linc-ROR silencing restrained cell proliferation and tumor growth (p < 0.01). Additionally, silenced Linc-ROR suppressed the immune escape of thyroid cancer cells and polarization of M2 macrophages (p < 0.01). Moreover, the PI3K/ AKT signaling mediated the action of silenced Linc-ROR on thyroid cancer proliferation, immune escape, and M2 macrophage polarization (p < 0.05). Linc-ROR may be a valuable target for thyroid cancer management. The limitations of this research are that the action of Linc-ROR on the tumor microenvironment has not been investigated in the animal model.