CSN5 Promotes Carcinogenesis of Thyroid Carcinoma Cells Through ANGPTL2
Author(s) -
Peiyi Xie,
Hui Wang,
Jiayu Fang,
Dongnian Du,
Ze Tian,
Jing Zhen,
Yue Liu,
Yongqi Ding,
Bidong Fu,
Fanrong Liu,
Da Huang,
Jichun Yu
Publication year - 2020
Publication title -
endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.674
H-Index - 257
eISSN - 1945-7170
pISSN - 0013-7227
DOI - 10.1210/endocr/bqaa206
Subject(s) - cop9 signalosome , thyroid carcinoma , carcinogenesis , thyroid , endocrinology , cancer research , carcinoma , medicine , metastasis , ubiquitin , protein subunit , cell growth , biology , cancer , biochemistry , enzyme , protease , peptide hydrolases , gene
COP9 signalosome subunit 5 (CSN5) plays a key role in carcinogenesis of multiple cancers and contributes to the stabilization of target proteins through deubiquitylation. However, the underlying role of CSN5 in thyroid carcinoma has not been reported. In this research, our data showed that CSN5 was overexpressed in thyroid carcinoma tissues compared with paracancerous tissues. Furthermore, a series of gain/loss functional assays were performed to demonstrate the role of CSN5 in facilitating thyroid carcinoma cell proliferation and metastasis. Additionally, we found there was a positive correlation between CSN5 and angiopoietin-like protein 2 (ANGPTL2) protein levels in thyroid carcinoma tissues and that CSN5 promoted thyroid carcinoma cell proliferation and metastasis through ANGPTL2. We also identified the underlying mechanism that CSN5 elevated ANGPTL2 protein level by directly binding it, decreasing its ubiquitination and degradation. Overall, our results highlight the significance of CSN5 in promoting thyroid carcinoma carcinogenesis and implicate CSN5 as a promising candidate for thyroid carcinoma treatment.
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