| First Author | Qiu B | Year | 2017 |
| Journal | Oncotarget | Volume | 8 |
| Issue | 5 | Pages | 8499-8511 |
| PubMed ID | 28036277 | Mgi Jnum | J:271676 |
| Mgi Id | MGI:6282901 | Doi | 10.18632/oncotarget.14293 |
| Citation | Qiu B, et al. (2017) DJ-1 promotes development of DEN-induced hepatocellular carcinoma and proliferation of liver cancer cells. Oncotarget 8(5):8499-8511 |
| abstractText | Chronic liver inflammation and injuries play a critical role in development of hepatocellular carcinoma (HCC). Parkinson disease (autosomal recessive, early onset) 7, encoding PARK7 protein (also called DJ-1), plays important roles in many carcinogenesis processes and is essential in modulating inflammation. However, whether DJ-1 is involved in HCC development remains largely unknown. To determine the effect of DJ-1 on HCC development, we accessed the correlation of hepatic DJ-1 expression with overall survival (OS) and TNM stage in 96 HCC patients and found a significant inverse correlation between DJ-1 expression and OS. By adopting a classic diethylnitrosamine (DEN)-induced murine HCC model, DJ-1 knockout (KO) mice displayed reduced tumorigenesis and cell proliferation, accompanied by decreased hepatic inflammation and IL-6/STAT3 activation. Furthermore, after an acute DEN challenge, DJ-1 KO mice showed significant decreases in liver injury, hepatocyte proliferation and DNA damage. In a human HCC cell line (MHCC-97L), cancer cell proliferation was induced by overexpression of DJ-1 and is related to oncogenic signaling of MAPKs and AKT. Induction of DJ-1 may serve as a novel regulator for HCC cell proliferation and HCC development possibly through enhanced MAPK signaling and inflammation. |
