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TRIP suppresses cell proliferation and invasion in choroidal melanoma via promoting the proteasomal degradation of Twist1
Author(s) -
Wei Chao,
Zhao Xiaofei,
Wang Lei,
Zhang Han
Publication year - 2020
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13882
Subject(s) - ubiquitin ligase , ubiquitin , gene knockdown , malignancy , cancer research , epithelial–mesenchymal transition , transcription factor , cell growth , in vitro , phenotype , melanoma , mesenchymal stem cell , protein degradation , microbiology and biotechnology , biology , chemistry , medicine , cell culture , pathology , cancer , metastasis , genetics , gene
Choroidal melanoma (CM) remains the most prevalent form of intraocular malignancy, and the prognosis of affected patients is poor. While the E3 ubiquitin ligase TRAF‐interacting protein (TRIP) is known to play key regulatory roles in multiple diseases, its relevance in CM remains uncertain. In the present study, we found that TRIP overexpression is sufficient to inhibit the proliferation, invasion, and epithelial–mesenchymal transition (EMT) of CM cells in vitro , whereas the opposite phenotypes are observed following TRIP knockdown. We further determined that TRIP is able to promote the K48‐polyubiquitination of EMT‐associated transcription factor Twist‐related protein 1, thereby suppressing EMT progression. Together, our results suggest that TRIP plays an important role in regulating the progression of CM and that it may therefore be an important therapeutic target for the treatment of this disease.