Suppression of CEP55 reduces cell viability and induces apoptosis in human lung cancer

Liu,Ligang; Mei,Qi; Zhao,Jing; Dai,Yuhong; Fu,Qiang

doi:10.3892/or.2016.5059

Suppression of CEP55 reduces cell viability and induces apoptosis in human lung cancer

Authors:
- Ligang Liu
- Qi Mei
- Jing Zhao
- Yuhong Dai
- Qiang Fu
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Affiliations: Department of Cardiothoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China, Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China
Published online on: August 31, 2016 https://doi.org/10.3892/or.2016.5059
Pages: 1939-1945

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Abstract

Centrosomal protein 55 (CEP55), identified as a centrosome‑associated protein, has been reported to be involved in human malignancies. However, its biological function in human lung cancer remains largely unknown. In the present study, we firstly analyzed the expression of CEP55 in 20 pairs of lung cancer and matched non‑tumor tissues using quantitative RT‑PCR analysis and found that CEP55 mRNA was significantly increased in lung cancer tissues compared with that in matched tumor‑adjacent tissues. Then we performed a loss‑of‑function assay using lung cancer cell lines A549 and 95D. Functionally, knockdown of CEP55 markedly inhibited cell viability and proliferation ability as determined by MTT and colony formation assays. Moreover, CEP55‑silenced cells were obviously arrested in the G0/G1 phase and presented significant cell apoptosis as determined using flow cytometric analysis. Mechanistically, western blot analysis further revealed that knockdown of CEP55 decreased the expression of CDK4, p21 and Bcl‑2, while it increased the expression of pro‑apoptotic protein, Bad, caspase‑3 and PARP in 95D cells. In conclusion, our data highlight the crucial role of CEP55 in promoting lung cancer cell proliferation in vitro and its inhibition may be a novel therapeutic strategy for lung cancer.

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