Knockdown of LINC00511 promotes radiosensitivity of thyroid carcinoma cells via suppressing JAK2/STAT3 signaling pathway.

Thyroid carcinoma is the most widespread malignancy in endocrine system with the increasing incidence. Despite of the advanced approaches to the management of thyroid carcinoma, the therapeutic effects remain unpleasant largely due to the radiosensitivity of thyroid carcinoma cells. LncRNAs play important part in the tumorigenesis and development, especially in the radiosensitivity of tumor cells. However, their roles in thyroid carcinoma still needed to be explored deeply. The purpose of our research is to inspect the possible biological role and regulation mechanism of LINC00511 desirable for therapies of thyroid carcinoma patients. In the present study, LINC00511 was significantly overexpressed in thyroid carcinoma and its silencing boosted radiosensitivity of thyroid carcinoma cells. Then we unveiled that LINC00511 regulated JAK2/STAT3 signaling pathway which was resistant to radiation treatment. Besides, TAF1 modulated JAK2 at transcriptional level. Moreover, LINC00511 bound to TAF1 and further promoted JAK2 expression. In conclusion, rescue experiments verified that the radiosensitivity of thyroid carcinoma cells was attributed to LINC00511/TAF1/JAK2/STAT3 axis. The current paper investigated the underlying mechanism of LINC00511 and set a new therapeutic direction for the therapy of thyroid carcinoma.