lncRNA LINC00673 induces proliferation, metastasis and epithelial-mesenchymal transition in thyroid carcinoma via Kruppel-like factor 2

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Abstract
The incidence of thyroid cancer has increased in the past decades; however, the underlying molecular mechanisms of thyroid cancer tumorigenesis remain unknown. Using sequencing technology, long intergenic non‑protein coding RNA 673 (LINC00673) was identified to be upregulated in several tumor tissues. However, the biological role of LINC00673 in thyroid carcinoma has yet to be determined. In this study, 60 matched pairs of thyroid tumor tissue and normal tissue were selected for study using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to validate previous findings; then, clinicopathologic features of the tissues were analyzed. Proliferation, colony formation, migration and invasion assays were performed, and epithelial-mesenchymal transition (EMT)-associated phenotypes were investigated following transfection with small interfering RNA to determine the specific role of LINC00673 in thyroid carcinoma cell lines (TPC1, KTC‑1 and BCPAP). The study revealed that long non‑coding RNA LINC00673 was significantly upregulated in thyroid cancer tissues compared with paired adjacent non‑tumor tissues using RT-qPCR and that high expression of LINC00673 is was associated with larger tumor size and lymph node metastasis in the validated cohort. Knockdown of LINC00673 inhibited cell proliferation and metastasis, whereas, LINC00673 overexpression had the opposite effect. The results showed that LINC00673 may influence EMT and the expression of Kruppel-like factor 2 (KLF2). Notably, KLF2 is considered a tumor suppressor gene in a variety of tumors. Finally, knock down of KLF2 enhanced thyroid carcinoma cell proliferation, and invasion and migration. In this study, the function of LINC00673 in promoting the proliferation and metastasis of thyroid carcinoma cell lines was identified, and LINC00673 may act as a novel therapeutic target for treating thyroid carcinoma.

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