Yuanqiang Lin1, Kailiang Cheng2, Tongtong Wang3, Qian Xie3, Minglong Chen3, Qianqian Chen4, Qiang Wen5. 1. Department of Ultrasonography, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, ErDao District, Changchun 13033, China. 2. Department of Radiology, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, ErDao District, Changchun 13033, China. 3. Department of Nuclear Medicine, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, ErDao District, Changchun 13033, China. 4. Department of Radiation Oncology, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, ErDao District, Changchun 13033, China. Electronic address: 39214306@qq.com. 5. Department of Nuclear Medicine, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, ErDao District, Changchun 13033, China. Electronic address: wenqiang54213@126.com.
Abstract
PURPOSE: The aims of this study were to test the influence of miR-217 on the proliferation, invasion, migration of thyroid cancer and the relevant mechanism. METHOD: miR-217 expression levels in thyroid cancer tissues and cell lines were detected by quantitative real-time PCR (qRT-PCR).Cell Counting Kit-8, flow cytometer, wound healing, transwell invasion assays were applied to evaluate the effect of miR-217 on proliferation, apoptosis, migration and invasion of thyroid cells. The luciferase reporter assay, qRT-PCR, and western blot were used to identify target of miR-217. Relative relationship of expression level between miR-217 and AKT3 was analyzed in thyroid cancer tissues. Xenograft transplantation was performed to test effect of miR-217 in vivo. RESULTS: We found that the expression of miR-217 was significantly decreased in thyroid cancer tissues cell lines. Significantly, decreased miR-217 expression were associated with the clinical stage and lymph node metastasis. Function studies revealed that miR-217 overexpression in thyroid cancer cells inhibited proliferation, migration, and invasion in vitro, as well as suppressed tumor growth in vivo. Subsequently, AKT3 was identified as a target of miR-217 in thyroid cancer. AKT3 expression was upregulated in thyroid cancer tissues, was inversely correlated with miR-217expression. Besides, overexpression of AKT3 efficiently abrogates suppressive effect on proliferation, migration and invasion in thyroid cancer cells caused by overexpression of miR-217. CONCLUSION: These data demonstrated a tumor suppressor role for miR-217 in thyroid cancer development and progression by targeting AKT3, suggesting miR-217 might be a potential target for thyroid cancer.
PURPOSE: The aims of this study were to test the influence of miR-217 on the proliferation, invasion, migration of thyroid cancer and the relevant mechanism. METHOD:miR-217 expression levels in thyroid cancer tissues and cell lines were detected by quantitative real-time PCR (qRT-PCR).Cell Counting Kit-8, flow cytometer, wound healing, transwell invasion assays were applied to evaluate the effect of miR-217 on proliferation, apoptosis, migration and invasion of thyroid cells. The luciferase reporter assay, qRT-PCR, and western blot were used to identify target of miR-217. Relative relationship of expression level between miR-217 and AKT3 was analyzed in thyroid cancer tissues. Xenograft transplantation was performed to test effect of miR-217 in vivo. RESULTS: We found that the expression of miR-217 was significantly decreased in thyroid cancer tissues cell lines. Significantly, decreased miR-217 expression were associated with the clinical stage and lymph node metastasis. Function studies revealed that miR-217 overexpression in thyroid cancer cells inhibited proliferation, migration, and invasion in vitro, as well as suppressed tumor growth in vivo. Subsequently, AKT3 was identified as a target of miR-217 in thyroid cancer. AKT3 expression was upregulated in thyroid cancer tissues, was inversely correlated with miR-217expression. Besides, overexpression of AKT3 efficiently abrogates suppressive effect on proliferation, migration and invasion in thyroid cancer cells caused by overexpression of miR-217. CONCLUSION: These data demonstrated a tumor suppressor role for miR-217 in thyroid cancer development and progression by targeting AKT3, suggesting miR-217 might be a potential target for thyroid cancer.