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NUAK2 沉默通过上调 CYFIP2 抑制宫颈癌细胞的增殖、迁移和上皮-间充质转化。

NUAK2 silencing inhibits the proliferation, migration and epithelial‑to‑mesenchymal transition of cervical cancer cells via upregulating CYFIP2.

机构信息

Department of Obstetrics and Gynecology, Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430010, P.R. China.

出版信息

Mol Med Rep. 2021 Nov;24(5). doi: 10.3892/mmr.2021.12457. Epub 2021 Sep 24.

DOI:10.3892/mmr.2021.12457
PMID:34558636
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8477169/
Abstract

NUAK family kinase 2 (NUAK2) has been reported to be involved in various cancer cell processes, including proliferation, apoptosis and invasion, by targeting multiple genes. However, to the best of our knowledge, its biological function in cervical cancer (CC) has not yet been elucidated. Therefore, the present study aimed to measure the expression of NUAK2 and to evaluate its functions in CC. The expression levels of NUAK2 and cytoplasmic FMRP‑interacting protein 2 (CYFIP2) were detected in CC tissues and cell lines. In addition, the effects of NUAK2 and CYFIP2 knockdown on CC cell proliferation, migration, invasion and epithelial‑to‑mesenchymal transition (EMT) were evaluated using Cell Counting Kit‑8, immunofluorescence, wound healing assay, Transwell assay and western blotting, respectively. Furthermore, co‑immunoprecipitation was performed to determine the interaction between NUAK2 and CYFIP2. The results revealed that the expression levels of NUAK2 were upregulated in CC tissues and cells, whereas CYFIP2 expression was reduced. In addition, knockdown of NUAK2 reduced cell proliferation, migration, invasion and EMT. Notably, NUAK2 was found to bind directly to CYFIP2. Furthermore, CYFIP2 inhibition reversed the effects of NUAK2 on CC cells. In summary, NUAK2 may regulate CYFIP2 expression to promote CC cell proliferation, migration, invasion and EMT.

摘要

NUAK 家族激酶 2(NUAK2)已被报道通过靶向多个基因参与多种癌细胞过程,包括增殖、凋亡和侵袭。然而,据我们所知,其在宫颈癌(CC)中的生物学功能尚未阐明。因此,本研究旨在测量 NUAK2 的表达并评估其在 CC 中的功能。检测了 CC 组织和细胞系中 NUAK2 和细胞质脆性 X 智力低下蛋白 2(CYFIP2)的表达水平。此外,使用细胞计数试剂盒-8、免疫荧光、划痕愈合试验、Transwell 试验和 Western blot 分别评估了 NUAK2 和 CYFIP2 敲低对 CC 细胞增殖、迁移、侵袭和上皮-间充质转化(EMT)的影响。此外,进行了共免疫沉淀以确定 NUAK2 和 CYFIP2 之间的相互作用。结果表明,NUAK2 在 CC 组织和细胞中的表达上调,而 CYFIP2 表达下调。此外,NUAK2 敲低可降低细胞增殖、迁移、侵袭和 EMT。值得注意的是,NUAK2 被发现直接与 CYFIP2 结合。此外,CYFIP2 抑制逆转了 NUAK2 对 CC 细胞的影响。综上所述,NUAK2 可能通过调节 CYFIP2 的表达来促进 CC 细胞的增殖、迁移、侵袭和 EMT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/6405b6fbd88e/mmr-24-05-12457-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/4038e1f680bb/mmr-24-05-12457-g00.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/852ec6ccf981/mmr-24-05-12457-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/85353d83d374/mmr-24-05-12457-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/1e7f3af27d07/mmr-24-05-12457-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/6405b6fbd88e/mmr-24-05-12457-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/4038e1f680bb/mmr-24-05-12457-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/9160d9e8553d/mmr-24-05-12457-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/852ec6ccf981/mmr-24-05-12457-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/85353d83d374/mmr-24-05-12457-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/1e7f3af27d07/mmr-24-05-12457-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4474/8477169/6405b6fbd88e/mmr-24-05-12457-g05.jpg

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