Abstract
Fos-related antigen 1 (Fra1) has been proposed as a gatekeeper of the mesenchymal-epithelial transition to epithelial-mesenchymal transition. Here, we showed that de-phosphorylated JNK2 increased the expression of Fra1 by promoting the expression of c-Jun and Jun-B. Conversely, phosphorylated JNK2 suppressed its expression via enhancing the ubiquitination of c-Jun and Jun-B. These data provided insights into the regulatory mechanism of JNK2 on the expression of Fra1. Our study thus demonstrated that the conversion of JNK2 from its phosphorylation to de-phosphorylation status promoted the switch of breast cancer cells from mesenchymal-epithelial transition to epithelial-mesenchymal transition.
Highlights
Epithelial-mesenchymal transition (EMT) is an important metastasis-associated process, in which cancer cells obtained the metastatic competence of migratory and invasive capabilities [1]
These results suggested that p-JNK1/2 may inhibit the expression of FRA1
To determine if the expression of Fos-related antigen 1 (Fra1) might generally correlate with the absence of p-JNK1/2, we extended these studies to murine breast cancer cell line (Figure 1B)
Summary
Epithelial-mesenchymal transition (EMT) is an important metastasis-associated process, in which cancer cells obtained the metastatic competence of migratory and invasive capabilities [1]. The molecular mechanisms regulating this complex process still need to be explored. A better understanding of this process is essential to develop new therapeutic strategies for cancer. The c-Jun N-terminal kinases (JNKs) can be activated by a range of stimuli and were labeled as “stress-activated protein kinases”. They are encoded by distinct genes [2,3,4]. All of 10 isoforms have the same phosphorylation site [2,3,4,5,6,7]
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