Critical role of c-Jun overexpression in liver metastasis of human breast cancer xenograft model

Abstract

Background: c-Jun/AP-1 has been linked to invasive properties of aggressive breast cancer. Recently, it has been reported that overexpression of c-Jun in breast cancer cell line MCF-7 resulted in increased AP-1 activity, motility and invasiveness of the cells in vitro and tumor formation in nude mice. However, the role of c-Jun in metastasis of human breast cancer in vivo is currently unknown.

Differential Up-regulation of MAP Kinase Phosphatases MKP3/DUSP6 and DUSP5 by Ets2 and c-Jun Converge in the Control of the Growth Arrest Versus Proliferation Response of MCF-7 Breast Cancer Cells to Phorbol Ester

“…These findings suggest a differential transcriptional control of MKP3 and DUSP5 by Ets2 and c-Jun, respectively, upon PMA stimulation of MCF-7 cells. Remarkably, both Ets2 and c-Jun activities have been associated with human breast cancer (62)(63)(64). In addition, the steady-state levels of MKP3 and DUSP5 proteins also seem to be differentially regulated in MCF-7 cells treated with PMA, the DUSP5 protein being more stable and/or more efficiently translated than the MKP3 protein.…”

14-3-3σ Gene Loss Leads to Activation of the Epithelial to Mesenchymal Transition Due to the Stabilization of c-Jun Protein

“…4). c-Jun expression is found to be elevated in multiple cancer types and is strongly associated with invasion and metastasis (53)(54)(55). c-Jun function can be regulated by the ERK pathway (52).…”

“…The AP1 transcription factor c-Jun has been shown to bind to the slug promoter, which can result in an increase in expression of slug and induction of EMT (52). c-Jun expression is found to be elevated in multiple cancer types and shows a significant association with invasion and metastasis (53)(54)(55). In epithelial cells, c-Jun is targeted for degradation by the proteasome, and multiple E3 ligases that mediate c-Jun ubiquitination, including COP1, ITCH, and FBW7, have been identified (56 -58).…”

Recovery of miR-139-5p in Ovarian Cancer Reverses Cisplatin Resistance by Targeting C-Jun

“…Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry c-Jun is an important component of the activation protein-1 (AP-1) transcription factor. In cancer cells, c-Jun functions as a proto-oncogene that promotes cell proliferation, invasion, and metastasis [39,40]. Moreover, overexpression of c-Jun can repair DNA damage, thus preventing the incidence of apoptosis in cancer cells [41,42].…”