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长链非编码 RNA SNAI3-AS1 通过诱饵 miR-27a-3p 和 miR-34a-5p 促进 PEG10 介导的肝癌增殖和转移。

LncRNA SNAI3-AS1 promotes PEG10-mediated proliferation and metastasis via decoying of miR-27a-3p and miR-34a-5p in hepatocellular carcinoma.

机构信息

Department of Gastroenterology, The First Affiliated Hospital of Xi'an Jiaotong University, 710061, Xi'an, Shaanxi, P. R. China.

出版信息

Cell Death Dis. 2020 Aug 11;11(8):685. doi: 10.1038/s41419-020-02840-z.

DOI:10.1038/s41419-020-02840-z
PMID:32826862
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7442791/
Abstract

During recent years, long noncoding RNAs (lncRNAs) have received focal attention due to their important function in cancer regulation. Though the relation between lncRNA SNAI3-AS1 and the development of hepatocellular carcinoma (HCC) has been described in our previous study, the role and the exact mechanism of SNAI3-AS1 are still unclear. In this study, qRT-PCR analysis revealed that the expression of SNAI3-AS1 was elevated and was correlated with the levels of PEG10 in HCC tissues. Through functional experiments, we determined that knockdown of SNAI3-AS1 and PEG10 inhibited the proliferation and metastasis, whereas overexpression of SNAI3-AS1 and PEG10 promoted the proliferation and metastasis of HCC cells. In addition, rescue experiments confirmed that upregulation of PEG10 partially restored cell function inhibition induced by SNAI3-AS1 knockdown. Therefore, we hypothesized that PEG10 may be regulated by SNAI3-AS1, which in turn mediates the malignant biological processes of HCC cells regulated by PEG10. Further bioinformatics analysis and mechanistic experiments showed that SNAI3-AS1 functions as a competing endogenous RNA (ceRNA) to activate PEG10 by acting as a sponge for miR-27-3p and miR-34a-5p. In summary, our study revealed that SNAI3-AS1 is a tumor regulator of PEG10 in the progression of HCC, and may contribute to the improvement of HCC diagnosis and therapy.

摘要

近年来，长非编码 RNA（lncRNA）因其在癌症调控中的重要功能而受到关注。虽然我们之前的研究已经描述了 lncRNA SNAI3-AS1 与肝细胞癌（HCC）发展之间的关系，但 SNAI3-AS1 的作用和确切机制仍不清楚。在这项研究中，qRT-PCR 分析显示 SNAI3-AS1 的表达升高，并与 HCC 组织中 PEG10 的水平相关。通过功能实验，我们确定敲低 SNAI3-AS1 和 PEG10 抑制了 HCC 细胞的增殖和转移，而过表达 SNAI3-AS1 和 PEG10 则促进了 HCC 细胞的增殖和转移。此外，挽救实验证实，上调 PEG10 部分恢复了 SNAI3-AS1 敲低引起的细胞功能抑制。因此，我们假设 PEG10 可能受 SNAI3-AS1 调控，进而介导 PEG10 调节的 HCC 细胞恶性生物学过程。进一步的生物信息学分析和机制实验表明，SNAI3-AS1 通过充当 miR-27-3p 和 miR-34a-5p 的海绵，作为竞争内源性 RNA（ceRNA）来激活 PEG10。总之，我们的研究揭示了 SNAI3-AS1 是 HCC 进展中 PEG10 的肿瘤调节剂，可能有助于改善 HCC 的诊断和治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/b2f51d5c7707/41419_2020_2840_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/53778d5057bb/41419_2020_2840_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/21ddd5bd0e5f/41419_2020_2840_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/62fd747f5d57/41419_2020_2840_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/d43ec8aedd4b/41419_2020_2840_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/047615c445d5/41419_2020_2840_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/3addd36af3ea/41419_2020_2840_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/b2f51d5c7707/41419_2020_2840_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/53778d5057bb/41419_2020_2840_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/21ddd5bd0e5f/41419_2020_2840_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/62fd747f5d57/41419_2020_2840_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/d43ec8aedd4b/41419_2020_2840_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/047615c445d5/41419_2020_2840_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/3addd36af3ea/41419_2020_2840_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9222/7442791/b2f51d5c7707/41419_2020_2840_Fig7_HTML.jpg

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