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SPC24 Regulates breast cancer progression by PI3K/AKT signaling
Juan Zhou1, Yunfeng Pei2, Geng Chen3
1The Affiliated XuZhou Hospital of Medical College of Southeast University, Xuzhou, People's Republic of China; Department of Medical Oncology, Affiliated to Medical College of Southeast University and Xuzhou Central Hospital, Xuzhou, People's Republic of China.
Abstract:
Breast cancer is a heterogeneous disease, presenting as several diverse clinical and histologic varieties and it is now the most frequently diagnosed cancer and is the sixth leading cause of cancer-related death in Chinese women. SPC24 is an important component of the mitotic checkpoint machinery and its carcinogenic roles have been shown in several cancers, including anaplastic thyroid cancer, hepatocellular carcinoma, and osteosarcoma. However, the role of SPC24 in breast cancer is still unclear. Here, we show SPC24 is highly expressed in breast cancer compared with the normal tissues. In addition, we observe that SPC24 knockdown can lead to attenuated cell growth, increased cell apoptosis and cell cycle progression. Consistent with the breast cancer cell results, the in vivo growth of the SPC24-knocking down cells was significantly inhibited. Interestingly, molecular analysis indicates that SPC24 regulates PI3K/AKT kinase pathway, indicating the important of SPC24 for clinical treatment. In aggregate, our results provide an oncogenic functionality of SPC24 in breast cancer progression.
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