NUAK2 silencing inhibits the proliferation, migration and epithelial‑to‑mesenchymal transition of cervical cancer cells via upregulating CYFIP2
- Yuxia Li
- Xiaohui Song
- Liping Liu
- Lei Yue
Affiliations: Department of Obstetrics and Gynecology, Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430010, P.R. China
- Published online on: September 22, 2021 https://doi.org/10.3892/mmr.2021.12457
Copyright: © Li
et al. This is an open access article distributed under the
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Commons Attribution License.
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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 in vitro 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.