Abstract
Although TC2N has proven to be an oncogene in lung cancer, its biological function and molecular mechanisms in other cancer still remains unclear. Here, we investigate in breast cancer that TC2N expression is sharply overexpressed in breast cancer specimens compared with normal breast specimens, and the low TC2N expression was associated with advanced stage, lymphatic metastasis, larger tumors and shorter survival time. Upregulation of TC2N significantly restrains breast cancer cell proliferation in vitro and tumor growth in vivo. Mechanistically, TC2N blocks AKT signaling in a PI3K dependent and independent way through weakening the interaction between ALK and p55γ or inhibiting the binding of EBP1 and AKT. To sum up, these results unmask an ambivalent role of TC2N in cancer, providing a promising inhibitor for PI3K-AKT signaling.
Highlights
Breast cancer (BC) is a huge growing public health problem and is the most common cancer in women worldwide[1]
We found that TC2N mRNA expression was significantly higher in BC tissues than in normal breast specimens (Fig. 1a)
These findings were further supported by detecting TC2N protein expression on a tissue microarray containing samples of 75 paired BC
Summary
Breast cancer (BC) is a huge growing public health problem and is the most common cancer in women worldwide[1]. Along with the enhancement and development of therapeutic methods and detection strategies, BC patient’s overall survival time is prolonged significantly, with a five-year survival rate of 90%2. TC2N is a putative C2 domain-containing protein that belongs to the carboxyl-terminal type (C-type) tandem C2 protein family[3]. The role of TC2N in cancer remains completely unexplored. We have identified TC2N as a novel oncogene that acts through suppression of the p53 signaling pathway in human lung cancer[4]. Due to the fact that many genes have a dual role in cancer[5,6], we intend to further explore the precise role of TC2N in cancer development and progression
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