RETRACTED: miR-137 acts as a tumor suppressor in papillary thyroid carcinoma by targeting CXCL12 (Retracted article. See vol. 46, 2021)

被引:46
作者
Dong, Su [1 ]
Jin, Meishan [2 ]
Li, Ye [3 ]
Ren, Peiyou [4 ]
Liu, Jia [4 ]
机构
[1] Jilin Univ, Hosp 1, Dept Anesthesia, Changchun 130021, Jilin, Peoples R China
[2] Jilin Univ, Hosp 1, Dept Pathol, Changchun 130021, Jilin, Peoples R China
[3] Jilin Univ, Hosp 1, Dept Radiol, Changchun 130021, Jilin, Peoples R China
[4] Jilin Univ, Hosp 1, Dept Thyroid Surg, 71 Xinmin St, Changchun 130021, Jilin, Peoples R China
关键词
papillary thyroid carcinoma; miR-137; CXCL12; proliferation; MICRORNA EXPRESSION; OVARIAN-CANCER; CELL-PROLIFERATION; LUNG-CANCER; GROWTH; ASSOCIATION; METASTASIS;
D O I
10.3892/or.2016.4604
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Accumulating evidence has shown that aberrantly expressed microRNAs (miRs) are extensively involved in tumorigenesis. microRNA-137 (miR-137) has been reported as a tumor suppressor in various types of cancer. However, the biological function and underlying molecular mechanism of miR-137 in papillary thyroid carcinoma (PTC) remain largely unknown. Therefore, the present study aimed to investigate the expression pattern of miR-137 and its functional significance in PTC. Quantitative RT-PCR (qRT-PCR) assay showed that miR-137 expression was significantly downregulated in human PTC tissues, and its expression was significantly negatively correlated with tumor-node-metastasis (TNM) stage and lymph node metastasis. Functional assays showed that forced expression of miR-137 in PTC cells significantly inhibited proliferation, colony formation, migration and invasion in vitro. Importantly, on the basis of bioinformatic analysis and luciferase reporter assay, we found that miR-137 directly targeted the 3'-untranslated region (3'-UTR) of C-X-C motif chemokine 12 (also known as SDF-1) (CXCL12). qRT-PCR and western blot analysis further verified the results and demonstrated that miR-137 could downregulate CXCL12 expression in PTC cells. We also confirmed that CXCL12 expression was increased in PTC tissues and was inversely correlated with miR-137. In addition, our results also showed that downregulation of CXCL12 mimicked the effects of miR-137 overexpression, and upregulation of CXCL12 partially reversed the inhibitory effects of miR-137 in PTC cells. These results showed that miR-137 may function as a tumor suppressor in PTC by targeting CXCL12, suggesting that miR-137 may act as a potential target for PTC treatment.
引用
收藏
页码:2151 / 2158
页数:8
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