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miR-331-3p 通过靶向 ST7L 在胰腺癌中发挥癌基因作用。

miR-331-3p functions as an oncogene by targeting ST7L in pancreatic cancer.

机构信息

Department of Gastroenterology, Wuhan Third Hospital, Tongren Hospital of Wuhan University, Wuhan, China.

Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.

出版信息

Carcinogenesis. 2018 Jul 30;39(8):1006-1015. doi: 10.1093/carcin/bgy074.

Abstract

Pancreatic cancer (PC) is a highly invasive tumor with early metastasis and poor prognosis, yet the mechanisms for tumor progression have not been fully elucidated. Emerging evidence indicates that microRNA-331-3p (miR-331-3p) plays an important role in the progression of diverse human cancers. Here, we found that miR-331-3p was significantly upregulated in tumor specimens of PC patients and PC cell lines. Functional studies showed that downregulation of miR-331-3p inhibited PC cell proliferation and epithelial-mesenchymal transition (EMT)-mediated metastasis in vitro. Furthermore, suppression of tumorigenicity 7 like (ST7L) was identified as a novel target gene of miR-331-3p. Tumor promotion effects of miR-331-3p were partially reversed by ST7L re-expression. In addition, miR-331-3p antagomir suppressed PC tumor growth and metastasis via upregulation of ST7L in xenograft mice. In summary, these results demonstrate that miR-331-3p is a tumor-promoting microRNA (miRNA) in PC cells and a promising biomarker for PC.

摘要

胰腺癌(PC)是一种具有早期转移和预后不良的高度侵袭性肿瘤,但肿瘤进展的机制尚未完全阐明。新出现的证据表明,微小 RNA-331-3p(miR-331-3p)在多种人类癌症的进展中发挥着重要作用。在这里,我们发现 miR-331-3p 在 PC 患者的肿瘤标本和 PC 细胞系中显著上调。功能研究表明,下调 miR-331-3p 抑制了 PC 细胞的增殖和体外上皮-间充质转化(EMT)介导的转移。此外,鉴定出肿瘤促进物 7 样(ST7L)是 miR-331-3p 的一个新的靶基因。通过 ST7L 的重新表达,部分逆转了 miR-331-3p 的促肿瘤作用。此外,miR-331-3p 拮抗剂通过在异种移植小鼠中上调 ST7L 抑制了 PC 肿瘤的生长和转移。总之,这些结果表明,miR-331-3p 是 PC 细胞中的一种促肿瘤 microRNA(miRNA),是 PC 的一种有前途的生物标志物。

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