- 作者: Wenbin Zhou, Hong Pan, Tiansong Xia, Jinqiu Xue, Lin Cheng, Ping Fan, Yifen Zhang, Weidong Zhu, Yi Xue, Xiaoan Liu, Qiang Ding, Yun Liu, Shui Wang
- 作者服務機構: Department of Breast Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China
- 中文摘要: --
- 英文摘要:
Background:
Our previous studies demonstrated that S100A16 promotes adipogenesis and is involved in weight gain attenuation induced by dietary calcium. Till now, the function of S100A16 in the breast cancer remains to be elucidated.
Results:
In this study, we observed that S100A16 was expressed in higher levels in human breast cancer tissues compared with paired adjacent non-cancerous tissues. Further examination showed that overexpression of S100A16 in MCF-7 cells could increase cell proliferation and colony formation. One major mechanistic change was that S100A16 was able to up-regulate the transcription factors Notch1, ZEB1, and ZEB2, which had the capacities to directly repress the expression of epithelial markers E-cadherin and β-catenin but increase mesenchymal markers N-cadherin and vimentin, a characterized phenotype of epithelialmensenchymal transition (EMT). In addition to display with morphologic change, migration and invasion were increased in S100A16 over-expressed MCF-7 cells. Importantly, knockdown of Notch1 by specific siRNA could reverse the EMT induced by S100A16
overexpression, which confirmed that Notch1 played a critical role in the process of EMT induced by S100A16.
Conclusions:
All together, our data indicated that S100A16 had a potential function to regulate some embryonic transcription factors to promote EMT in breast cancer cells which may be an important target site for the therapy of breast cancer. - 中文關鍵字: --
- 英文關鍵字: Breast cancer, S100A16, EMT, Notch1, MCF-7