Department of Digestion, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Hematological Disease Engineering Center of Ministry of Education, Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Int J Mol Med. 2019 Apr;43(4):1817-1829. doi: 10.3892/ijmm.2019.4107. Epub 2019 Feb 25.
Previous studies have demonstrated that the dysregulation of microRNAs (miRs) is frequently associated with cancer progression. Deregulation of miR‑106b‑3p has been observed in various types of human cancer. However, the biological function of miR‑106b‑3p in esophageal squamous cell carcinoma (ESCC) remains unclear. Thus, the aim of this study was to investigate the role of miR‑106b‑3p in ESCC. In the current study, the results indicated that miR‑106b‑3p was upregulated in ESCC cell lines and tissues. An increase in miR‑106b‑3p using miR mimics significantly promoted the proliferation of ESCC cells in vitro. Furthermore, the results demonstrated that miR‑106b‑3p overexpression promoted migration, invasion and epithelial‑mesenchymal transition (EMT) of ESCC cells. In addition, zinc and ring finger 3 (ZNRF3) was identified as a target of miR‑106b‑3p in ESCC cells, and the ZNRF3 expression level was inversely associated with miR‑106b‑3p. It was also demonstrated that miR‑106b‑3p has a role in EMT by regulating Wnt/β‑catenin signaling pathway in ESCC. In conclusion, these data suggested that miR‑106b‑3p promotes cell proliferation and invasion, partially by downregulating ZNRF3 and inducing EMT via Wnt/β‑catenin signaling in ESCC cells. Thus, miR‑106b‑3p and ZNRF3 may be novel molecular targets for the future treatment of ESCC.
先前的研究表明，microRNAs（miRs）的失调常常与癌症的进展有关。miR-106b-3p 的失调已在多种人类癌症中观察到。然而，miR-106b-3p 在食管鳞状细胞癌（ESCC）中的生物学功能尚不清楚。因此，本研究旨在探讨 miR-106b-3p 在 ESCC 中的作用。在本研究中，结果表明 miR-106b-3p 在 ESCC 细胞系和组织中上调。使用 miR 模拟物增加 miR-106b-3p 水平显著促进 ESCC 细胞在体外的增殖。此外，结果表明 miR-106b-3p 的过表达促进 ESCC 细胞的迁移、侵袭和上皮-间充质转化（EMT）。此外，锌指蛋白 3（ZNRF3）被鉴定为 ESCC 细胞中 miR-106b-3p 的靶基因，ZNRF3 的表达水平与 miR-106b-3p 呈负相关。还表明 miR-106b-3p 通过调节 ESCC 细胞中的 Wnt/β-catenin 信号通路在 EMT 中发挥作用。总之，这些数据表明 miR-106b-3p 通过下调 ZNRF3 并通过 Wnt/β-catenin 信号诱导 EMT 促进 ESCC 细胞的增殖和侵袭，部分发挥作用。因此，miR-106b-3p 和 ZNRF3 可能是未来 ESCC 治疗的新的分子靶点。
