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CiRS-7 通过调控 miR-7/HOXB13 促进食管鳞癌细胞的生长和转移。

CiRS-7 promotes growth and metastasis of esophageal squamous cell carcinoma via regulation of miR-7/HOXB13.

机构信息

Department of General Medicine, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.

Department of Emergency Medicine, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.

出版信息

Cell Death Dis. 2018 Aug 6;9(8):838. doi: 10.1038/s41419-018-0852-y.

DOI:10.1038/s41419-018-0852-y
PMID:30082829
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6079012/
Abstract

The circular RNA ciRS-7 has been reported to be involved in the pathogenesis of various tumors, including gastric and colorectal cancer. However, the role of ciRS-7 in esophageal squamous cell carcinoma (ESCC) remains unsolved. In this study, we found that the ciRS-7 expression was significantly upregulated in ESCC cancer tissues compared with matched normal tissues and associated with poor patient survival. Overexpression of ciRS-7 abrogated the tumor-suppressive roles of miR-7 including cell proliferation, migration and invasion in vitro as well as tumor growth and lung metastasis in vivo. Mechanistically, ciRS-7 functioned as the sponge of miR-7 and reactivated its downstream HOXB13-mediated NF-κB/p65 pathway. Conclusively, our findings demonstrate how ciRS-7 induces malignant progression of ESCC and that ciRS-7 may act as a novel prognostic marker and therapeutic target for this lethal disease.

摘要

环状 RNA ciRS-7 已被报道参与多种肿瘤的发病机制,包括胃癌和结直肠癌。然而,ciRS-7 在食管鳞状细胞癌(ESCC)中的作用仍未解决。在本研究中,我们发现 ciRS-7 在 ESCC 癌组织中的表达明显高于匹配的正常组织,并与患者生存不良相关。ciRS-7 的过表达可消除 miR-7 的肿瘤抑制作用,包括体外的细胞增殖、迁移和侵袭以及体内的肿瘤生长和肺转移。机制上,ciRS-7 作为 miR-7 的海绵,重新激活其下游 HOXB13 介导的 NF-κB/p65 通路。总之,我们的研究结果表明 ciRS-7 如何诱导 ESCC 的恶性进展,ciRS-7 可能成为这种致命疾病的新的预后标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/b7c9bb3f27f6/41419_2018_852_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/364969abaac0/41419_2018_852_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/55f938e9f3ed/41419_2018_852_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/407376585c3f/41419_2018_852_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/a50d5e81eb21/41419_2018_852_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/f7f183f955b1/41419_2018_852_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/4b68c80d932f/41419_2018_852_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/b7c9bb3f27f6/41419_2018_852_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/364969abaac0/41419_2018_852_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/55f938e9f3ed/41419_2018_852_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/407376585c3f/41419_2018_852_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/a50d5e81eb21/41419_2018_852_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/f7f183f955b1/41419_2018_852_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/4b68c80d932f/41419_2018_852_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ce/6079012/b7c9bb3f27f6/41419_2018_852_Fig7_HTML.jpg

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