Downregulation of NIMA-related kinase-7 inhibits cell proliferation by inducing cell cycle arrest in human retinoblastoma cells
- Jian Zhang
- Li Wang
- Yongkang Zhang
Affiliations: Department of Ophthalmology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China, Department of Ophthalmology, Ankang City Central Hospital, Ankang, Shaanxi 725000, P.R. China, Department of Ophthalmology, Shaanxi Provincial Rehabilitation Hospital, Xi'an, Shaanxi 710065, P.R. China
- Published online on: November 23, 2017 https://doi.org/10.3892/etm.2017.5558
Copyright: © Zhang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
NIMA-related kinase-7 (Nek7) is a centrosomal kinase involved in various types of cancer, including gallbladder cancer and hepatocellular carcinoma. However, the biological function and the potential underlying mechanism of Nek7 in retinoblastoma remain largely unknown. Therefore, the present study investigated the effects of Nek7 in retinoblastoma cells. The expression of Nek7 was initially determined and observed to be commonly upregulated in retinoblastoma cell lines (Y79, SO‑RB50 and WERI‑RB1) as compared with that in normal retinal pigment epithelium cells. Next, the endogenous expression of Nek7 was efficiently knocked down in Y79 and SO‑RB50 cells using a lentivirus‑mediated RNA interference approach, as confirmed by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Loss‑of‑function assays, including MTT, colony formation and flow cytometry, indicated that knockdown of Nek7 significantly inhibited cell growth, impaired the colony formation ability and induced cell cycle arrest at G0/G1 phase. Furthermore, mechanistic studies demonstrated that silencing of Nek7 resulted in reduced cyclin‑dependent kinase 2, cyclin D1 and cyclin E levels in vitro. In conclusion, the present study highlights the crucial role of Nek7 in promoting retinoblastoma cell proliferation, and Nek7‑silencing may serve as a novel therapeutic target for retinoblastoma.