최재훈
2017-10-13T06:27:32Z
2017-10-13T06:27:32Z
2015-12
ONCOGENE, v. 34, NO 50, Page. 6055-6065
0950-9232
1476-5594
http://www.nature.com/onc/journal/v34/n50/full/onc201554a.html?foxtrotcallback=true
http://hdl.handle.net/20.500.11754/29623
Extracellular Matrix Protein 1 (ECM1) is a marker for tumorigenesis and is correlated with invasiveness and poor prognosis in various types of cancer. However, the functional role of ECM1 in cancer metastasis is unclear. Here, we detected high ECM1 level in breast cancer patient sera that was associated with recurrence of tumor. The modulation of ECM1 expression affected not only cell migration and invasion, but also sphere-forming ability and drug resistance in breast cancer cell lines. In addition, ECM1 regulated the gene expression associated with the epithelial to mesenchymal transition (EMT) progression and cancer stem cell (CSC) maintenance. Interestingly, ECM1 increased beta-catenin expression at the post-translational level through induction of MUC1, which was physically associated with beta-catenin. Indeed, the association between beta-catenin and the MUC1 cytoplasmic tail was increased by ECM1. Furthermore, forced expression of beta-catenin altered the gene expression that potentiated EMT progression and CSC phenotype maintenance in the cells. These data provide evidence that ECM1 has an important role in cancer metastasis through beta-catenin stabilization.
This work was supported by an NRF grant (2013-059143) from the Korea Research Foundation and Converging Research Center Program (2014048814).
en
NATURE PUBLISHING GROUP
EXTRACELLULAR-MATRIX PROTEIN-1
NF-KAPPA-B
EPITHELIAL-MESENCHYMAL TRANSITION
BREAST-CANCER CELLS
STEM-CELLS
LYMPHATIC METASTASIS
SIGNALING PATHWAYS
INITIATING CELLS
SELF-RENEWAL
EXPRESSION
ECM1 regulates tumor metastasis and CSC-like property through stabilization of beta-catenin
Article
50
34
10.1038/onc.2015.54
6055-6065
ONCOGENE
Lee, K-m
Nam, K.
Oh, S.
Lim, J.
Kim, R. K.
Shim, D.
Choi, J-h
Lee, S-J
Yu, J-H
Lee, J. W.
2015000098
S
COLLEGE OF NATURAL SCIENCES[S]
DEPARTMENT OF LIFE SCIENCE
jchoi75
R-6224-2016
http://orcid.org/0000-0002-5265-3463