Knockdown of Aurora-B inhibits the growth of non-small cell lung cancer A549 cells | Zendy

Jing Yu | Zendy; Long Zhou | Zendy; Tian Zhao | Zendy; Wei Bai | Zendy; Jing Zhou | Zendy; Wei Zhang | Zendy

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Knockdown of Aurora-B inhibits the growth of non-small cell lung cancer A549 cells

Author(s) -

Jing Yu,

Long Zhou,

Tian Zhao,

Wei Bai,

Jing Zhou,

Wei Zhang

Publication year - 2015

Publication title -

oncology letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.766

H-Index - 54

eISSN - 1792-1082

pISSN - 1792-1074

DOI - 10.3892/ol.2015.3467

Subject(s) - gene knockdown , a549 cell , cancer research , oncogene , pi3k/akt/mtor pathway , apoptosis , lung cancer , gene silencing , cell cycle , aurora b kinase , protein kinase b , cell growth , aurora inhibitor , cancer , biology , cell , microbiology and biotechnology , chemistry , signal transduction , medicine , cell division , biochemistry , spindle apparatus , gene

Elevated expression of Aurora-B affects cell apoptosis and proliferation in a variety of solid tumors. However, the role of Aurora-B has been poorly evaluated in non-small cell lung cancer (NSCLC). In the present study, it was found that Aurora-B was overexpressed in tissue specimens obtained from 174 patients with lung cancer. It was also demonstrated that knockdown of Aurora-B induces apoptosis and inhibits the growth of lung cancer A549 cells in vitro and in vivo . Furthermore, it was found that silencing Aurora-B decreased the activity of the phosphoinositide 3-kinase (PI3K)/AKT pathway. Therefore, it was concluded that knockdown of Aurora-B induces apoptosis and inhibits growth in NSCLC A549 cells, in addition to inhibiting the activity of the PI3K/AKT signaling pathway. Targeting Aurora-B may provide a novel target for lung cancer therapy.

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