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长链非编码 RNA GAS6-AS1 通过 miR-370-3p/miR-1296-5p 和 FUS 调控 TRIM14 促进结直肠癌的发生发展和转移。

LncRNA GAS6-AS1 facilitates tumorigenesis and metastasis of colorectal cancer by regulating TRIM14 through miR-370-3p/miR-1296-5p and FUS.

机构信息

Department of Oncology, Jingjiang People's Hospital, The Seventh Affiliated Hospital of Yangzhou University, Jingjiang, Jiangsu, China.

Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.

出版信息

J Transl Med. 2022 Aug 12;20(1):356. doi: 10.1186/s12967-022-03550-0.

DOI:10.1186/s12967-022-03550-0
PMID:35962353
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9373365/
Abstract

BACKGROUND

Long non-coding RNAs (lncRNAs) are essential regulators of tumorigenesis and the development of colorectal cancer (CRC). Here, we aimed to investigate the role of lncRNA GAS6-AS1 in CRC and its potential mechanisms.

METHODS

Bioinformatics analyses evaluated the level of GAS6-AS1 in colon cancer, its correlation with clinicopathological factors, survival curve and diagnostic value. qRT-PCR were performed to detect the GAS6-AS1 level in CRC samples and cell lines. The CCK8, EdU, scratch healing, transwell assays and animal experiments were conducted to investigate the function of GAS6-AS1 in CRC. RNA immunoprecipitation (RIP) and dual-luciferase reporter gene analyses were carried out to reveal interaction between GAS6-AS1, TRIM14, FUS, and miR-370-3p/miR-1296-5p.

RESULTS

GAS6-AS1 was greatly elevated in CRC and positively associated with unfavorable prognosis of CRC patients. Functionally, GAS6-AS1 positively regulates CRC proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and induces CRC growth and metastasis in vivo. Moreover, GAS6-AS1 exerted oncogenic function by competitively binding to miR-370-3p and miR-1296-5p, thereby upregulating TRIM14. Furthermore, we verified that GAS6-AS1 and TRIM14 both interact with FUS and that GAS6-AS1 stabilized TRIM14 mRNA by recruiting FUS. Besides, rescue experiments furtherly demonstrated that GAS6-AS1 facilitate progression of CRC by regulating TRIM14.

CONCLUSION

Collectively, these findings demonstrate that GAS6-AS1 promotes TRIM14-mediated cell proliferation, migration, invasion, and EMT of CRC via ceRNA network and FUS-dependent manner, suggesting that GAS6-AS1 could be utilized as a novel biomarker and therapeutic target for CRC.

摘要

背景

长链非编码 RNA（lncRNA）是肿瘤发生和结直肠癌（CRC）发展的重要调节因子。在这里，我们旨在研究 lncRNA GAS6-AS1 在 CRC 中的作用及其潜在机制。

方法

生物信息学分析评估了 GAS6-AS1 在结肠癌中的水平、与临床病理因素的相关性、生存曲线和诊断价值。qRT-PCR 用于检测 CRC 样本和细胞系中的 GAS6-AS1 水平。CCK8、EdU、划痕愈合、Transwell 测定和动物实验用于研究 GAS6-AS1 在 CRC 中的功能。RNA 免疫沉淀（RIP）和双荧光素酶报告基因分析用于揭示 GAS6-AS1、TRIM14、FUS 和 miR-370-3p/miR-1296-5p 之间的相互作用。

结果

GAS6-AS1 在 CRC 中显著上调，与 CRC 患者的不良预后呈正相关。功能上，GAS6-AS1 可正向调节 CRC 细胞的增殖、迁移、侵袭和上皮间质转化（EMT），并在体内诱导 CRC 的生长和转移。此外，GAS6-AS1 通过竞争性结合 miR-370-3p 和 miR-1296-5p 发挥致癌作用，从而上调 TRIM14。此外，我们验证了 GAS6-AS1 和 TRIM14 均与 FUS 相互作用，GAS6-AS1 通过募集 FUS 稳定 TRIM14 mRNA。此外，挽救实验进一步表明，GAS6-AS1 通过调节 TRIM14 促进 CRC 的进展。

结论

总之，这些发现表明，GAS6-AS1 通过 ceRNA 网络和 FUS 依赖性方式促进 TRIM14 介导的 CRC 细胞增殖、迁移、侵袭和 EMT，提示 GAS6-AS1 可作为 CRC 的新型生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3638/9373365/1c8be33b3d87/12967_2022_3550_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3638/9373365/1c8be33b3d87/12967_2022_3550_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3638/9373365/67a80f3648b9/12967_2022_3550_Fig1_HTML.jpg
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