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Peroxiredoxin-2 represses melanoma metastasis by increasing E-cadherin/β-catenin complexes in adherens junctions

Title
Peroxiredoxin-2 represses melanoma metastasis by increasing E-cadherin/β-catenin complexes in adherens junctions
Authors
Lee D.J.Kang D.H.Choi M.Choi Y.J.Lee J.Y.Park J.H.Park Y.J.Lee K.W.Kang S.W.
Ewha Authors
강상원이두재박윤정
SCOPUS Author ID
강상원scopus; 이두재scopus; 박윤정scopus
Issue Date
2013
Journal Title
Cancer Research
ISSN
0008-5472JCR Link
Citation
vol. 73, no. 15, pp. 4744 - 4757
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
In melanoma, transition to the vertical growth phase is the critical step in conversion to a deadly malignant disease. Here, we offer the first evidence that an antioxidant enzyme has a key role in this transition.Wefound that the antioxidant enzyme peroxiredoxin-2 (Prx2) inversely correlated with the metastatic capacity of human melanoma cells. Silencing Prx2 expression stimulated proliferation and migration, whereas ectopic expression of Prx2 produced the opposite effect. Mechanistic investigations indicated that Prx2 negatively regulated Src/ERK activation status, which in turn fortified adherens junctions function by increasing E-cadherin expression and phospho-Y654- dependent retention of β-catenin in the plasma membrane. In murine melanoma cells, Prx2 silencing enhanced lung metastasis in vivo. Interestingly, the natural compound gliotoxin, which is known to exert a Prx-like activity, inhibited proliferation and migration as well as lung metastasis of Prx2-deficient melanoma cells. Overall, our findings reveal that Prx2 is a key regulator of invasion and metastasis in melanoma, and also suggest a pharmacologic strategy to effectively decrease deadly malignant forms of this disease. © 2013 American Association for Cancer Research.
DOI
10.1158/0008-5472.CAN-12-4226
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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