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Vol 50(2016) N 5 p. 725-730; DOI 10.1134/S0026893316030043 Full Text

Y. Cai1, J. He2, D. Zhang1*

Suppression of long non-coding RNA CCAT2 improves tamoxifen-resistant breast cancer cells' response to tamoxifen

1Department of Geriatric Oncology, The General Hospital of Chinese People's Liberation Army, Beijing City, P. R. China
2Department of Geriatric Integrated Surgery, The General Hospital of Chinese People's Liberation Army, Beijing City, P. R. China

*zhangdzhangd301@163.com
Received - 2015-08-28; Accepted - 2015-10-01

Breast cancer is one of the most common cancers in women worldwide. Tamoxifen (TAM) provided a successful treatment for ER-positive (ER+) breast cancer for many years. However, ER+ patients with metastatic diseases respond poorly to TAM therapy and many initial responders eventually relapse. Emerging evidence indicates that long non-coding RNAs (lncRNAs) may have a critical role in the regulation of cellular processes such as cancer progression and metastasis, though the function of lncRNAs in TAM-resistance is still unclear. To investigate the role of CCAT2 in the development of resistance to TAM treatment of breast cancer, we established TAM-resistant models in MCF-7 and T47D cells. The present study demonstrates that TAM-resistant cells show a higher level of CCAT2 expression compared with TAM-sensitive cells. Biologically, CCAT2 knockdown could inhibit proliferation and induce apoptosis in TAM-resistant cells exposed to TAM. Furthermore, knockdown of CCAT2 improves the sensitivity to TAM in TAM-resistant cells. Overall, the study results provide a novel therapeutic approach for TAM-resistant patients through depleting CCAT2 expression.

long non-coding RNAs, CCAT2, breast cancer, tamoxifen resistance



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