Department of Medical Oncology, Institute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, 38 Guangji Road, Hangzhou, 310022, Zhejiang, China.
Department of Breast Surgery, Zhejiang Cancer Hospital, 38 Guangji Road, Hangzhou, 310012, Zhejiang, China.
In Vitro Cell Dev Biol Anim. 2020 Aug;56(7):550-558. doi: 10.1007/s11626-020-00499-6. Epub 2020 Aug 28.
MiR-183 is a tumor onco-miR and has been shown by our previous studies to be overexpressed in esophageal squamous cell carcinomas (ESCCs). In this study, we sought to determine the possible mechanisms of miR-183 in ESCC. In our study, cell migration and invasion, real-time PCR, Western blot, and chromatin immunoprecipitation (ChIP) assays were used to explore the mechanism of miR-183 in three ESCC cell lines. We found several potential transcription factors, including c-Jun, by bioinformatics methods. Using a ChIP assay, we identified that c-Jun binds to the promoter region of pre-miR-183 and that upregulated c-Jun expression is related to increased expression of miR-183. We found that downregulation of miR-183 significantly reduced the cell invasiveness and migration of ESCC cells, whereas upregulation of miR-183 via a mimic increased the cell migration and invasion of ESCC cells. We further discovered one direct miR-183 target gene, Smad4, which has been implicated in invasion and metastasis. Furthermore, miR-183 promoted epithelial-mesenchymal transition (EMT), which is involved in the invasion and migration of ESCC cells. Dysregulation of miR-183 has an important role in tumor growth and invasion because miR-183 targets Smad4. Therefore, suppression of miR-183 may provide a potential approach for treatment.
miR-183 是一种肿瘤致癌 miRNA,我们之前的研究表明它在食管鳞状细胞癌(ESCC)中过表达。在这项研究中,我们试图确定 miR-183 在 ESCC 中的可能机制。在我们的研究中,使用细胞迁移和侵袭、实时 PCR、Western blot 和染色质免疫沉淀(ChIP)测定来探索三种 ESCC 细胞系中 miR-183 的机制。我们通过生物信息学方法发现了几个潜在的转录因子,包括 c-Jun。通过 ChIP 测定,我们确定 c-Jun 结合到 pre-miR-183 的启动子区域,上调的 c-Jun 表达与 miR-183 的表达增加有关。我们发现下调 miR-183 显著降低了 ESCC 细胞的侵袭和迁移能力,而通过模拟物上调 miR-183 则增加了 ESCC 细胞的迁移和侵袭能力。我们进一步发现了一个直接的 miR-183 靶基因 Smad4,它与侵袭和转移有关。此外,miR-183 促进了上皮-间充质转化(EMT),这涉及 ESCC 细胞的侵袭和迁移。miR-183 的失调在肿瘤生长和侵袭中起着重要作用,因为 miR-183 靶向 Smad4。因此,抑制 miR-183 可能为治疗提供一种潜在的方法。