American Association for Cancer Research
00085472can121045-sup-t1_96k.pdf (96.57 kB)

Supplementary Table 1 from SOX4 Induces Epithelial–Mesenchymal Transition and Contributes to Breast Cancer Progression

Download (96.57 kB)
journal contribution
posted on 2023-03-30, 21:21 authored by Jianchao Zhang, Qian Liang, Yang Lei, Min Yao, Lili Li, Xiaoge Gao, Jingxin Feng, Yu Zhang, Hongwen Gao, Dong-Xu Liu, Jun Lu, Baiqu Huang

PDF file - 96K, New data of Oncomine analysis of SOX4 expression in human breast cancer tissues in comparison with normal breast tissues



Epithelial–mesenchymal transition (EMT) is a developmental program, which is associated with breast cancer progression and metastasis. Here, we report that ectopic overexpression of SOX4 in immortalized human mammary epithelial cells is sufficient for acquisition of mesenchymal traits, enhanced cell migration, and invasion, along with epithelial stem cell properties defined by the presence of a CD44high/CD24low cell subpopulation. SOX4 positively regulated expression of known EMT inducers, also activating the TGF-β pathway to contribute to EMT. SOX4 itself was induced by TGF-β in mammary epithelial cells and was required for TGF-β–induced EMT. Murine xenograft experiments showed that SOX4 cooperated with oncogenic Ras to promote tumorigenesis in vivo. Finally, in clinical specimens of human breast cancer, we found that SOX4 was abnormally overexpressed and correlated with the triple-negative breast cancer subtype (ER−/PR−/HER2−). Our findings define an important function for SOX4 in the progression of breast cancer by orchestrating EMT, and they implicate this gene product as a marker of poor prognosis in this disease. Cancer Res; 72(17); 4597–608. ©2012 AACR.