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微小 RNA-138 通过靶向信号素 4C 对乳腺癌细胞上皮-间充质转化和侵袭的影响。

Effect of microrna-138 on epithelial-Mesenchymal transition and invasion of breast cancer cells by targeting semaphorin 4C.

机构信息

Second Ward of Breast Surgery, Shanxi Cancer Hospital, TaiYuan, China.

Third Ward of Thoracic Surgery, Shanxi Cancer Hospital, TaiYuan, China.

出版信息

Bioengineered. 2021 Dec;12(2):10117-10125. doi: 10.1080/21655979.2021.2000733.

DOI:10.1080/21655979.2021.2000733
PMID:34747314
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8809962/
Abstract

In view of the role of miR-138 in cancer cells, we predicted the target of miR-138 and its targeting to SEMA4C by bioinformatics software and luciferase experiment. The expression levels of miR-138 in human normal breast epithelial cells and two kinds of BC cells were compared, and the transfection cells were selected. MiR-138 mimetic negative control (miR-NC), miR-138 mimic and miR-138 inhibitor were designed for cell transfection. The results showed that the expression level of miR-138 in MCF-7 cells was the lowest. The up regulation of miR-138 would lead to the high expression of E-cad and the low expression of N-cad, vim and SEMA4C, and the vitality and invasion of BC cells would decrease. The down regulation of miR-138 would lead to the low expression of E-cad and the high expression of N-cad, vim and SEMA4C, and the vitality and invasion of BC cells would increase. miR-138 targeted regulation of SEMA4C can promote the expression of N-cad, inhibit the expression of E-cad, vim and SEMA4C, reverse the EMT of BC cells, and inhibit the activity and invasion of BC cells. MiR-138 has clinical potential as a tumor marker of BC.

摘要

鉴于 miR-138 在癌细胞中的作用,我们通过生物信息学软件和荧光素酶实验预测了 miR-138 的靶标及其对 SEMA4C 的靶向作用。比较了 miR-138 在人正常乳腺上皮细胞和两种 BC 细胞中的表达水平,并选择了转染细胞。设计了 miR-138 模拟物阴性对照(miR-NC)、miR-138 模拟物和 miR-138 抑制剂进行细胞转染。结果表明,MCF-7 细胞中 miR-138 的表达水平最低。miR-138 的上调会导致 E-cad 的高表达和 N-cad、vim 和 SEMA4C 的低表达,BC 细胞的活力和侵袭性降低。miR-138 的下调会导致 E-cad 的低表达和 N-cad、vim 和 SEMA4C 的高表达,BC 细胞的活力和侵袭性增加。miR-138 对 SEMA4C 的靶向调节可以促进 N-cad 的表达,抑制 E-cad、vim 和 SEMA4C 的表达,逆转 BC 细胞的 EMT,并抑制 BC 细胞的活性和侵袭性。miR-138 具有作为 BC 肿瘤标志物的临床潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/cb6dc7a80e76/KBIE_A_2000733_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/1f73bb0f0ca0/KBIE_A_2000733_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/bc8e555f9377/KBIE_A_2000733_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/24fffabfae30/KBIE_A_2000733_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/e3fd74629312/KBIE_A_2000733_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/cb6dc7a80e76/KBIE_A_2000733_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/1f73bb0f0ca0/KBIE_A_2000733_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/bc8e555f9377/KBIE_A_2000733_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/24fffabfae30/KBIE_A_2000733_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/e3fd74629312/KBIE_A_2000733_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70fa/8809962/cb6dc7a80e76/KBIE_A_2000733_F0005_OC.jpg

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