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信号素3C的沉默抑制MCF-7乳腺癌细胞的增殖和迁移。

Silencing of semaphorin 3C suppresses cell proliferation and migration in MCF-7 breast cancer cells.

作者信息

Zhu Xiaofang, Zhang Xiangjian, Ye Zhiqiang, Chen Yizuo, Lv Lin, Zhang Xiaohua, Hu Hongye

机构信息

Department of Rheumatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.

Department of Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.

出版信息

Oncol Lett. 2017 Nov;14(5):5913-5917. doi: 10.3892/ol.2017.6920. Epub 2017 Sep 8.

DOI:10.3892/ol.2017.6920
PMID:29113226
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5661468/
Abstract

Previous studies have suggested that semaphorin 3C (SEMA3C) is involved in the tumorigenesis and metastasis of a number of types of cancer. The aim of the present study was to investigate the role of SEMA3C in the proliferation and migration of MCF-7 breast cancer cells. Small interfering (si)RNA sequences targeting SEMA3C were constructed and transfected into MCF-7 cells in order to silence the expression of SEMA3C. Cell proliferation and migration were measured using CCK-8 and Transwell assays, respectively. Transfection with SEMA3C siRNA significantly downregulated the expression of SEMA3C in MCF-7 cells, and significantly suppressed cell proliferation and migration. Therefore, SEMA3C-targeted siRNA may be of potential use for the early diagnosis and treatment of breast cancer.

摘要

先前的研究表明,信号素3C(SEMA3C)参与多种类型癌症的肿瘤发生和转移。本研究的目的是探讨SEMA3C在MCF-7乳腺癌细胞增殖和迁移中的作用。构建了靶向SEMA3C的小干扰(si)RNA序列并转染到MCF-7细胞中,以沉默SEMA3C的表达。分别使用CCK-8和Transwell检测法测量细胞增殖和迁移。用SEMA3C siRNA转染可显著下调MCF-7细胞中SEMA3C的表达,并显著抑制细胞增殖和迁移。因此,靶向SEMA3C的siRNA可能对乳腺癌的早期诊断和治疗具有潜在用途。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/a503ac4c9f09/ol-14-05-5913-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/c25af6ea74e3/ol-14-05-5913-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/bbcb88025822/ol-14-05-5913-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/6328024d256c/ol-14-05-5913-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/a503ac4c9f09/ol-14-05-5913-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/c25af6ea74e3/ol-14-05-5913-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/bbcb88025822/ol-14-05-5913-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/6328024d256c/ol-14-05-5913-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee8e/5661468/a503ac4c9f09/ol-14-05-5913-g03.jpg

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本文引用的文献

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Notch1 signaling regulates the epithelial-mesenchymal transition and invasion of breast cancer in a Slug-dependent manner.Notch1信号通路以依赖Slug的方式调节乳腺癌的上皮-间质转化和侵袭。
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The potential of class 3 semaphorins as both targets and therapeutics in cancer.
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