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长链非编码 RNA SNHG6 通过海绵吸附 miR-4465 促进卵巢透明细胞癌细胞增殖和迁移。

Long non-coding RNA SNHG6 promotes cell proliferation and migration through sponging miR-4465 in ovarian clear cell carcinoma.

机构信息

Department of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China.

Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China.

出版信息

J Cell Mol Med. 2019 Aug;23(8):5025-5036. doi: 10.1111/jcmm.14359. Epub 2019 May 22.

DOI:10.1111/jcmm.14359
PMID:31119871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6653241/
Abstract

Dysregulation of small nucleolar RNA host gene 6 (SNHG6) exerts critical oncogenic effects and facilitates tumourigenesis in human cancers. However, little information about the expression pattern of SNHG6 in ovarian clear cell carcinoma (OCCC) is available, and the contributions of this long non-coding RNA to the tumourigenesis and progression of OCCC are unclear. In the present study, we showed via quantitative real-time PCR that SNHG6 expression was abnormally up-regulated in OCCC tissues relative to that in unpaired normal ovarian tissues. High SNHG6 expression was correlated with vascular invasion, distant metastasis and poor survival. Further functional experiments demonstrated that knockdown of SNHG6 in OCCC cells inhibited cell proliferation, migration and invasion in vitro as well as tumour growth in vivo. Moreover, SNHG6 functioned as a competing endogenous RNA (ceRNA), effectively acting as a sponge for miR-4465 and thereby modulating the expression of enhancer of zeste homolog 2 (EZH2). Taken together, our data suggest that SNHG6 is a novel molecule involved in OCCC progression and that targeting the ceRNA network involving SNHG6 may be a treatment strategy in OCCC.

摘要

小核仁 RNA 宿主基因 6(SNHG6)失调在人类癌症中发挥关键致癌作用并促进肿瘤发生。然而,关于 SNHG6 在卵巢透明细胞癌(OCCC)中的表达模式的信息很少,并且这种长非编码 RNA 对 OCCC 的肿瘤发生和进展的贡献尚不清楚。在本研究中,我们通过实时定量 PCR 显示 SNHG6 在 OCCC 组织中的表达相对于未配对的正常卵巢组织异常上调。高 SNHG6 表达与血管侵犯、远处转移和不良预后相关。进一步的功能实验表明,在 OCCC 细胞中敲低 SNHG6 可抑制体外细胞增殖、迁移和侵袭以及体内肿瘤生长。此外,SNHG6 作为竞争性内源 RNA(ceRNA)发挥作用,可有效充当 miR-4465 的海绵,从而调节胚胎外胚层发育蛋白 2(EZH2)的表达。总之,我们的数据表明 SNHG6 是参与 OCCC 进展的新分子,靶向涉及 SNHG6 的 ceRNA 网络可能是 OCCC 的一种治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/713f72b6f9ad/JCMM-23-5025-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/b68aaa7aec8b/JCMM-23-5025-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/0b3396e1c4c3/JCMM-23-5025-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/473630490674/JCMM-23-5025-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/f6183a6d2abf/JCMM-23-5025-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/d166a834727c/JCMM-23-5025-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/176196c6303e/JCMM-23-5025-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/713f72b6f9ad/JCMM-23-5025-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/b68aaa7aec8b/JCMM-23-5025-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/0b3396e1c4c3/JCMM-23-5025-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/473630490674/JCMM-23-5025-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/f6183a6d2abf/JCMM-23-5025-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/d166a834727c/JCMM-23-5025-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/176196c6303e/JCMM-23-5025-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe31/6653241/713f72b6f9ad/JCMM-23-5025-g007.jpg

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