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miR-455 通过靶向作用于结直肠癌中的 GATA6 发挥肿瘤抑制作用。

miR-455 Functions as a Tumor Suppressor Through Targeting GATA6 in Colorectal Cancer.

机构信息

Cancer Biotherapy Center and Oncology Department, Baotou Tumor Hospital, Clinical Oncology of Baotou Medical College, Baotou, Inner Mongolia, P.R. China.

Department of Central Laboratory, The First Affiliated Hospital of Baotou Medical College, Baotou, Inner Mongolia, P.R. China.

出版信息

Oncol Res. 2019 Feb 21;27(3):311-316. doi: 10.3727/096504018X15220579006875. Epub 2018 Apr 3.

DOI:10.3727/096504018X15220579006875
PMID:29615149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7848416/
Abstract

Emerging evidence indicates that microRNAs (miRNAs) are often aberrantly expressed in human cancers. Meanwhile, the importance of miRNAs in regulating multiple cellular biological processes has been appreciated. The aim of this study was to investigate the significance of miR-455 and identify its possible mechanism in regulating colorectal cancer (CRC) progression. We found that the expression of miR-455 was sharply reduced in CRC tissues and cell lines. Importantly, the low expression of miR-455 was associated with poor overall survival of CRC patients. Overexpression of miR-455 in CRC cell lines significantly inhibited cell proliferation and migration in vitro. Moreover, GATA-binding protein 6 (GATA6), whose expression can be inversely regulated by miR-455 in CRC cell lines, was validated as a direct target of miR-455. Overall, our results revealed that miR-455 functions as a tumor suppressor, and its downregulation may contribute to CRC progression. Our study may provide a novel therapeutic target for CRC in the future.

摘要

新出现的证据表明,microRNAs(miRNAs)在人类癌症中经常异常表达。同时,miRNAs 在调节多种细胞生物学过程中的重要性也得到了认可。本研究旨在探讨 miR-455 的意义,并确定其在调节结直肠癌(CRC)进展中的可能机制。我们发现 miR-455 在 CRC 组织和细胞系中的表达明显降低。重要的是,miR-455 的低表达与 CRC 患者的总生存率差相关。在 CRC 细胞系中过表达 miR-455 可显著抑制体外细胞增殖和迁移。此外,GATA 结合蛋白 6(GATA6)的表达可被 miR-455 在 CRC 细胞系中反向调节,其被验证为 miR-455 的直接靶标。总体而言,我们的研究结果表明 miR-455 作为一种肿瘤抑制因子发挥作用,其下调可能导致 CRC 的进展。我们的研究可能为未来的 CRC 提供新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/5f7fba1dfd03/OR-27-311-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/40b4a47de78e/OR-27-311-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/e99a160e8217/OR-27-311-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/ec8c1cd6dcfa/OR-27-311-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/5f7fba1dfd03/OR-27-311-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/40b4a47de78e/OR-27-311-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/e99a160e8217/OR-27-311-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/ec8c1cd6dcfa/OR-27-311-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dab6/7848416/5f7fba1dfd03/OR-27-311-g004.jpg

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