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MicroRNA-409 通过靶向特异性富含 AT 序列结合蛋白 1(SATB1)调节乳腺癌细胞系的增殖和侵袭。

MicroRNA-409 regulates the proliferation and invasion of breast cancer cell lines by targeting special AT-rich sequence-binding protein 1 (SATB1).

机构信息

Department of Anesthesiology, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.

Research Center and Tumor Research Institute, the Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.

出版信息

Bioengineered. 2022 May;13(5):13045-13054. doi: 10.1080/21655979.2022.2073320.

DOI:10.1080/21655979.2022.2073320
PMID:35611599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275908/
Abstract

This study aims to determine the cellular functions and clinical significance of microRNA-409 (miR-409) in breast cancer by targeting special AT-rich sequence-binding protein 1 (SATB1). Breast cancer tissues and adjacent normal tissues, breast cancer cell lines (MDA-MB-453, MDA-MB-231, BT-549, BR3, and MCF-7) were used. miR-409 mimics, miR-409 inhibitor, SATB1, and siSATB1 were transiently transduced into cancer cells independently or together. RT-qPCR, Western blot, Cell Counting Kit-8 (CCK8), and Transwell assays were carried out to analyze the expression, cellular proliferation, and invasion. The results showed that the expression of miR-409 in breast cancer tissues is lower than that in adjacent tissues. The application of a target prediction algorithm predicts that the candidate gene regulated by miR-409 may be SATB1. The expression level of miR-409 in MDA-MB-453 cells is lower, while in BT-549 cells it is higher, when compared with MDA-MB-231, BR3, and MCF-7. The proliferation rate and invasive ability of MDA-MB-453 cells transfected with the miR-409 mimic was significantly lower than that of the miRNA negative control (miR-NC) cells, while the proliferation rate and invasive ability of BT-549 cells transfected with the miR-409 inhibitor were significantly increased. Cell proliferation and invasion of miR-409 mimic and SATB1 co-transfected MDA-MB-453 cells increased compared with that of miR-409 mimic-transfected cells, while miR-409 inhibitor and siSATB1 co-transfected BT-549 cells showed the opposite result. All these results indicated that miR-409 regulates breast cancer proliferation and invasion by targeting SATB1 and might be a potential therapeutic target for the treatment of breast cancer.

摘要

本研究旨在通过靶向特殊富含 AT 序列结合蛋白 1(SATB1)来确定 microRNA-409(miR-409)在乳腺癌中的细胞功能和临床意义。使用乳腺癌组织和相邻正常组织、乳腺癌细胞系(MDA-MB-453、MDA-MB-231、BT-549、BR3 和 MCF-7)。分别或共同瞬时转染 miR-409 模拟物、miR-409 抑制剂、SATB1 和 siSATB1 进入癌细胞。进行 RT-qPCR、Western blot、细胞计数试剂盒-8(CCK8)和 Transwell 测定,以分析表达、细胞增殖和侵袭。结果表明,乳腺癌组织中 miR-409 的表达低于相邻组织。靶预测算法的应用预测 miR-409 调节的候选基因可能是 SATB1。与 MDA-MB-231、BR3 和 MCF-7 相比,MDA-MB-453 细胞中的 miR-409 表达水平较低,而 BT-549 细胞中的 miR-409 表达水平较高。转染 miR-409 模拟物的 MDA-MB-453 细胞的增殖率和侵袭能力明显低于 miRNA 阴性对照(miR-NC)细胞,而转染 miR-409 抑制剂的 BT-549 细胞的增殖率和侵袭能力明显增加。与转染 miR-409 模拟物的细胞相比,miR-409 模拟物和 SATB1 共转染的 MDA-MB-453 细胞的细胞增殖和侵袭增加,而 miR-409 抑制剂和 siSATB1 共转染的 BT-549 细胞则表现出相反的结果。所有这些结果表明,miR-409 通过靶向 SATB1 调节乳腺癌的增殖和侵袭,可能成为治疗乳腺癌的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/1f090a002a2e/KBIE_A_2073320_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/697983b93c70/KBIE_A_2073320_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/d5af66c65a06/KBIE_A_2073320_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/f4ac186d88be/KBIE_A_2073320_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/ee94b1f390d0/KBIE_A_2073320_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/d5440c3a7772/KBIE_A_2073320_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/1f090a002a2e/KBIE_A_2073320_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/697983b93c70/KBIE_A_2073320_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/d5af66c65a06/KBIE_A_2073320_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/f4ac186d88be/KBIE_A_2073320_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/ee94b1f390d0/KBIE_A_2073320_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/d5440c3a7772/KBIE_A_2073320_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/938c/9275908/1f090a002a2e/KBIE_A_2073320_F0005_OC.jpg

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