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长非编码 RNA Lnc-408 通过调节 LIMK1 促进乳腺癌细胞的侵袭和转移。

Long non-coding RNA Lnc-408 promotes invasion and metastasis of breast cancer cell by regulating LIMK1.

机构信息

Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing, China.

Experimental Teaching & Lab Management Center, Chongqing Medical University, Chongqing, China.

出版信息

Oncogene. 2021 Jun;40(24):4198-4213. doi: 10.1038/s41388-021-01845-y. Epub 2021 Jun 2.

DOI:10.1038/s41388-021-01845-y
PMID:34079084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8211561/
Abstract

Invasion and metastasis are the leading causes of death in patients with breast cancer (BC), and epithelial-mesenchymal transformation (EMT) plays an essential role in this process. Here, we found that Lnc-408, a novel long noncoding RNA (lncRNA), is significantly upregulated in BC cells undergoing EMT and in BC tumor with lymphatic metastases compared with those without lymphatic metastases. Lnc-408 can enhance BC invasion and metastasis by regulating the expression of LIMK1. Mechanistically, Lnc-408 serves as a sponge for miR-654-5p to relieve the suppression of miR-654-5p on its target LIMK1. Knockdown or knockout of Lnc-408 in invasive BC cells clearly decreased LIMK1 levels, and ectopic Lnc-408 in MCF-7 cells increased LIMK1 expression to promote cell invasion. Lnc-408-mediated enhancement of LIMK1 plays a key role in cytoskeletal stability and promotes invadopodium formation in BC cells via p-cofilin/F-actin. In addition, the increased LIMK1 also facilitates the expression of MMP2, ITGB1, and COL1A1 by phosphorylating CREB. In conclusion, our findings reveal that Lnc-408 promotes BC invasion and metastasis via the Lnc-408/miR-654-5p/LIMK1 axis, highlighting a novel promising target for the diagnosis and treatment of BC.

摘要

浸润和转移是乳腺癌（BC）患者死亡的主要原因，上皮-间质转化（EMT）在这个过程中起着重要作用。在这里，我们发现，与无淋巴转移的 BC 肿瘤相比，发生 EMT 的 BC 细胞和有淋巴转移的 BC 肿瘤中，新型长非编码 RNA（lncRNA）Lnc-408 显著上调。Lnc-408 可以通过调节 LIMK1 的表达来增强 BC 的侵袭和转移。在机制上，Lnc-408 作为 miR-654-5p 的海绵，减轻 miR-654-5p 对其靶标 LIMK1 的抑制作用。在侵袭性 BC 细胞中敲低或敲除 Lnc-408 明显降低 LIMK1 水平，而 MCF-7 细胞中的外源性 Lnc-408 增加 LIMK1 表达以促进细胞侵袭。Lnc-408 介导的 LIMK1 增强在 BC 细胞中的细胞骨架稳定性中起关键作用，并通过 p-cofilin/F-actin 促进侵袭小体的形成。此外，增加的 LIMK1 还通过磷酸化 CREB 促进 MMP2、ITGB1 和 COL1A1 的表达。总之，我们的研究结果表明，Lnc-408 通过 Lnc-408/miR-654-5p/LIMK1 轴促进 BC 的侵袭和转移，为 BC 的诊断和治疗提供了一个新的有希望的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/9b1128fefca7/41388_2021_1845_Fig8_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/8838745e11e1/41388_2021_1845_Fig5_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/30f78b082974/41388_2021_1845_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/9b1128fefca7/41388_2021_1845_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/55a56f205597/41388_2021_1845_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/92518b5986a0/41388_2021_1845_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/e89bcb472638/41388_2021_1845_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/2d4a890c0363/41388_2021_1845_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/8838745e11e1/41388_2021_1845_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/50c0a0edc3fe/41388_2021_1845_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/30f78b082974/41388_2021_1845_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ceb/8211561/9b1128fefca7/41388_2021_1845_Fig8_HTML.jpg

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