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Long non-coding RNA BRM (lncBRM) was first identified in liver cancer stem cells and was reported to promote multiple cancer types. However, the function of lncBRM in papillary thyroid carcinoma (PTC) remains unclear. The primary focus of the present study was to determine the biological role of lncBRM in PTC. Reverse transcription-quantitative PCR assays revealed that lncBRM was upregulated in PTC tissues and cells. Cell Counting Kit-8, Transwell invasion and colony-formation assays were performed to assess cell proliferation, invasion and migration, respectively. Furthermore, high expression of lncBRM was associated with poor overall survival time in patients with PTC. lncBRM knockout significantly suppressed cell proliferation, migration and invasion. lncBRM was predicted to bind to microRNA (miR)-331-3p and targets SLC25A1. Overexpression of miR-331-3p or inhibition of SLC25A1 resulted in significantly suppressed proliferation, migration and invasion of PTC cells. Rescue assays demonstrated that inhibition of miR-331-3p significantly abrogated the effects of lncBRM knockout on PTC cell proliferation, migration and invasion. In conclusion, the present study suggests that lncBRM promotes PTC by regulating miR-331-3p and targeting SLC25A1.

Long non‑coding RNA BRM promotes proliferation and invasion of papillary thyroid carcinoma by regulating the microRNA‑331‑3p/SLC25A1 axis