TMEM2 expression is down-regulated in liver tissues of patients with chronic hepatitis B virus (HBV) infection and HepG2.2.15 cells carrying HBV genomic DNA. In the present study, the researchers further explored the effects of TMEM2 on HepG2 and HepG2.2.15 cells during HBV infection and its mechanism. By using lentiviral vectors, the researchers established HepG2 shTMEM2 cells with stable knockdown of TMEM2 as well as HepG2 TMEM2 and HepG2.2.15 TMEM2 cells with stable overexpression of TMEM2. The results showed that TMEM2 expression was reduced in HBV-infected liver tissues and HepG2.2.15 cells. In TMEM2 knockdown HepG2 shTMEM2 cells, HBsAg, HBcAg, HBV DNA, and HBV cccDNA levels were significantly increased, whereas these levels were significantly decreased in HepG2 TMEM2 and HepG2.2.15 TMEM2 cells overexpressing TMEM2. The findings suggest that TMEM2 inhibits HBV infection in HepG2 and HepG2.2.15 cells through activation of the JAK-STAT signaling pathway.
Figure 1. Effects of TMEM2 overexpression or silencing on HBsAg, HBcAg, HBV DNA, and HBV cccDNA levels after HBV infection in HepG2 cell lines with stable GFP expression. (Zhu X, et al., 2016)
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I used the GFP Stable Cell Line HepG2 product in the experiment. Due to its unique labeling characteristics, this product enables the expressed cell lines to be efficiently expressed not only in liver cell research, but also in multiple clinical fields, providing a broader exploration space.
United Kingdom
04/03/2020
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