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长链非编码RNA LINC00963通过海绵化miR-324-3p并诱导ACK1表达促进乳腺癌的肿瘤发生和放射抗性。

LncRNA LINC00963 Promotes Tumorigenesis and Radioresistance in Breast Cancer by Sponging miR-324-3p and Inducing ACK1 Expression.

作者信息

Zhang Na, Zeng Xue, Sun Chaonan, Guo Hong, Wang Tianlu, Wei Linlin, Zhang Yaotian, Zhao Jiaming, Ma Xinchi

机构信息

Department of Radiation Oncology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, China.

Department of Radiation Oncology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, China.

出版信息

Mol Ther Nucleic Acids. 2019 Dec 6;18:871-881. doi: 10.1016/j.omtn.2019.09.033. Epub 2019 Oct 22.

DOI:10.1016/j.omtn.2019.09.033
PMID:31751910
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6881674/
Abstract

Upregulation of long non-coding RNA LINC00963 has been observed in several cancer types. In this study, we analyzed the clinical and biological significance of LINC00963 in breast cancer. The key microRNA (miR) mediating the action of LINC00963 was identified. We show that LINC00963 upregulation is correlated with aggressive parameters of breast cancer. Silencing of LINC00963 suppresses the proliferation and tumorigenesis of breast cancer cells, whereas LINC00963 overexpression exerts an opposite effect. Knockdown of LINC00963 enhances DNA damage and oxidative stress and sensitizes breast cancer cells to radiation. Mechanistically, LINC00963 antagonizes the repressive activity of miR-324-3p on ACK1 expression. Clinically, there is a negative correlation between miR-324-3p and LINC00963 expression in breast cancer tissues. Overexpression of LINC00963 or ACK1 rescues the inhibitory effects of miR-324-3p on breast cancer cell proliferation and radiosensitivity. In addition, knockdown of ACK1 attenuates LINC00963-dependent breast cancer growth and tumorigenesis. Taken together, LINC00963 promotes tumorigenesis and radioresistance in breast cancer through interplay with miR-324-3p and derepression of ACK1. LINC00963 may represent a potential target for the treatment of breast cancer.

摘要

在多种癌症类型中均观察到长链非编码RNA LINC00963的上调。在本研究中，我们分析了LINC00963在乳腺癌中的临床和生物学意义。确定了介导LINC00963作用的关键微小RNA（miR）。我们发现LINC00963的上调与乳腺癌的侵袭性参数相关。沉默LINC00963可抑制乳腺癌细胞的增殖和肿瘤发生，而LINC00963的过表达则产生相反的效果。敲低LINC00963可增强DNA损伤和氧化应激，并使乳腺癌细胞对辐射敏感。机制上，LINC00963拮抗miR-324-3p对ACK1表达的抑制活性。临床上，乳腺癌组织中miR-324-3p与LINC00963表达呈负相关。LINC00963或ACK1的过表达可挽救miR-324-3p对乳腺癌细胞增殖和放射敏感性的抑制作用。此外，敲低ACK1可减弱LINC00963依赖的乳腺癌生长和肿瘤发生。综上所述，LINC00963通过与miR-324-3p相互作用并解除对ACK1的抑制，促进乳腺癌的肿瘤发生和放射抗性。LINC00963可能是乳腺癌治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/8ddde7b685c7/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/01f89bb7de38/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/6cd262856b6c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/c10a3558eb0c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/682cc3168262/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/09cd0f9d424f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/d60e14d0e4f1/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/80fd94349af5/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/8ddde7b685c7/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/01f89bb7de38/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/1ec558f8643a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/6cd262856b6c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/c10a3558eb0c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/682cc3168262/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/09cd0f9d424f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/d60e14d0e4f1/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/80fd94349af5/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca8f/6881674/8ddde7b685c7/gr9.jpg

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