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The BTB domain protein‐Cul3 complex is a novel regulator of Collagen expression in Breast Cancer
Author(s) -
kim kyungho,
Kim YounJae
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.802.38
Subject(s) - breast cancer , ubiquitin ligase , cancer research , metastasis , regulator , downregulation and upregulation , ubiquitin , cancer cell , microbiology and biotechnology , cancer , biology , chemistry , gene , biochemistry , genetics
CUL3‐RING ubiquitin ligases are associated with diverse cellular processes through over two hundred BTB‐domain proteins. RHOBTB3, a BTB‐domain protein, harbors capable of assembling Cullin3‐ dependent ubiquitin ligase complexes and recent studies have been suggested to play an essential role in transport vesicle docking at the Golgi complex. Collagen type I alpha 1(Col1A1) reportedly associated with tumor interstitial macromolecular transport and cancer cell dissemination. However, the precise function and mechanism of Col1A1 remain unclear how Col1A1 is regulated in human breast cancer growth and metastasis. To address this question, we analysed RHOBTB3 and Col1A1 gene expression in breast cancer using the public database. We exemplify each three representative studies showing RHOBTB3 and Col1A1 are generally upregulated in breast cancer. To determine the effects of RHOBTB3 and Col1A1 expression on metastasis and involvement of RHOBTB3 and Col1A1, we performed knock‐down of RHOBTB3 in breast cancer cells. The knock‐down of RHOBTB3 significantly decreased expression of COL1A1 mRNA and protein and inhibition of cell growth and invasion in breast cancer. Collectively, these findings demonstrated RHOBTB3 is an important factor for regulation of the COL1A1 synthesis and inhibition of cell growth and invasion in breast cancer cells. Thus, RHOBTB3 is oncogenic and a potential oncotarget for breast cancer therapy. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .