Abstract
The co-chaperone ERdj3/DNAJB11 is involved in the endoplasmic reticulum stress response observed in cancer cells. We hypothesized that ERdj3 functions as a hepatocellular carcinoma (HCC) oncogene by inhibiting AATZ degradation. ERdj3 and AATZ expressions were analyzed in 84 HCC patients. Cell proliferation, epithelial-mesenchymal transition marker expression, migration and invasiveness were assessed in HepG2 and Huh-7 cells. A murine xenograft tumor model was constructed. ERdj3 is upregulated in HCC tumors and cell lines. Tumor ERdj3 levels are positively associated with cirrhosis, enhanced HCC status, inferior survival outcomes and AATZ levels. ERdj3 suppresses AATZ degradation. ERdj3 overexpression enhances proliferation, epithelial-mesenchymal transition marker expression, migration, invasiveness and xenograft tumor growth in an AATZ-dependent manner. ERdj3 enhances HCC progression through suppressing AATZ degradation.
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