NAC1 promotes the migration of prostate cancer cells and participates in osteoclastogenesis by negatively regulating IFNβ

Chen,Fang; Yin,Yinghao; Yan,Zhifeng; Cao,Ke; Zhong,Kuangbiao

doi:10.3892/ol.2017.7670

NAC1 promotes the migration of prostate cancer cells and participates in osteoclastogenesis by negatively regulating IFNβ

Authors:
- Fang Chen
- Yinghao Yin
- Zhifeng Yan
- Ke Cao
- Kuangbiao Zhong
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Affiliations: Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China, Department of Oncology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China
Published online on: December 20, 2017 https://doi.org/10.3892/ol.2017.7670
Pages: 2921-2928
Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Nucleus accumbens-associated protein 1 (NAC1), a transcriptional co‑regulator, is overexpressed in advanced prostate cancer. However, the NAC1‑regulated transcriptome has not been completely explored. In the present study, the functional silencing of NAC1 blocked the migration of prostate cancer cells and suppress osteoclastogenesis. The present study also determined that NAC1 was overexpressed in the highly aggressive prostate cancer cell lines PC‑3, DU‑145 and LNCaP. NAC1 small interfering RNA treatment of DU‑145 cells decreased cell migration, but interestingly had no significant effects on cell proliferation. Furthermore, microarray analysis showed that a group of genes may be associated with the development of prostate cancer after NAC1 knockdown, including interferon‑β (IFNβ), which is reported to be involved in osteoclastogenesis, an important factor affecting bone metastasis. The mechanisms of NAC1 function were further explored by co‑culture studies using PC‑3 and RAW264.7 osteoclast precursor cells, which demonstrated that silencing NAC1 downregulated the genes associated with the activation of osteoclasts. Furthermore, it was revealed that NAC1 had the ability to affect the release of IFNβ into the extracellular environment. Together, these findings indicated that NAC1 promoted cell migration, and that NAC1 may have a key role in osteoclastogenesis.

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