Overexpression of 14-3-3θ promotes tumor metastasis and indicates poor prognosis in breast carcinoma
Metrics: PDF 2841 views | HTML 2536 views | ?
Nanlin Li1,*, Hui Wang1,*, Jing Fan1, Chao Tong1, Jixin Yang1, Hongliang Wei1, Jun Yi1, Rui Ling1
1 Department of Vascular and Endocrine Surgery, Xijing Hospital, The Fourth Military Medical University, Xi’an, Shaanxi, China
* These authors contributed equally to the work
Rui Ling, email:
Nanlin Li, email:
Keywords: 14-3-3θ, Breast Cancer, Metastasis, Prognosis
Received: October 14, 2013 Accepted: December 3, 2013 Published: December 5, 2013
An isoform of the 14-3-3 protein family, 14-3-3θ has been linked with tumor cell proliferation and apoptosis. However, the role of 14-3-3θ in the progression of breast cancer remains unknown. Here, we report that 14-3-3θ plays a critical role in breast cancer metastasis and prognosis. The expression of 14-3-3θ was markedly higher in breast cancer tissues compared to adjacent normal tissues. A hospital-based study cohort of 216 breast cancer patients was evaluated in this study. The level of 14-3-3θ expression was determined and correlated based upon tumor clinicopathological features, disease-free survival, and overall survival. We found that overexpression of 14-3-3θ was correlated with advanced TNM stage (P < 0.05), lymph node metastasis (P < 0.05), and ER negative status (P < 0.05). Breast cancer patients with high 14-3-3θ expression had a shorter overall survival and a higher rate of recurrence than those with low 14-3-3θ expression. Additionally, knockdown of 14-3-3θ expression in breast cancer cells inhibited metastasis in vitro. Similarly, an in vivo assay showed that 14-3-3θ knockdown dramatically suppressed the growth of breast cancer xenografts and inhibited tumor cell metastasis in a lung metastasis model. Thus, this study provided the first evidence that 14-3-3θ is a novel tumor suppressor and may serve as a candidate prognostic biomarker and target for new therapies in metastatic breast cancer.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.