Editorial on “Transcription factor SPZ1 promotes TWIST-mediated epithelial—mesenchymal transition and oncogenesis in human liver cancer”
Twist1, a basic helix-loop-helix (bHLH) transcription factor, has been implicated in epithelial mesenchymal transitions (EMTs) in a variety of cancers including lung cancer (1-3). As a result, Twist1 is thought to play an important role in metastasis through a variety of described mechanisms (4-9). In addition, overexpression of Twist1 is associated with chemotherapy resistance and is associated with poor prognosis (3,10-12). Twist1 overexpression is also associated with cancer stemness, a phenotype thought to be responsible for cancer initiation, metastasis, and therapy resistance (2). Twist1 is an attractive target in cancer because it is overexpressed in cancer while minimally expressed in normal tissues. Although small inhibitory RNA suppression of Twist1 has been effective in reducing cancer growth in vitro, therapies targeting Twist1 that can be used in vivo have not yet been reported. As a result, understanding the regulation of Twist1 may reveal new ways of blocking Twist1 expression that may lead to new effective cancer therapies.