Effect of GPX4 knockdown on gene expression profile of EBV positive gastric cancer cell line AGS-EBV.
Reactive oxygen species (ROS) mediated oxidative stress plays an increasingly extensive role in tumorigenesis. Oxidative stress is also an important mechanism for host cells to resist infection by pathogenic microorganisms. Viruses have a similar defense mechanism. Studies have shown that ROS levels are elevated during in vitro and in vivo EBV infection. In nasopharyngeal carcinoma, EBV latent membrane protein LMP1 "REDOX" nasopharyngeal carcinoma cells by up-regulating NRF2 and NOX2, acquiring new REDOX homeostasis to tolerate higher levels of ROS. In gastric cancer, EBV upregulates NOX2 by down-regulating miR34a via EBNA1, thereby enhancing the antioxidant capacity of host cells. In addition, oxidative stress is involved in the lytic reactivation of EBV, but the specific mechanism is not clear. GPX4 is an important ROS scavenger that plays a role in maintaining cellular REDOX homeostasis. Our study showed that GPX4 is relatively highly expressed in EBV-positive gastric cancer cell lines, which can promote tumor proliferation and migration, and we found that GPX4 helps maintain latent infection of EBV in gastric cancer. In order to further explore the specific mechanism, we performed transcriptome sequencing analysis after knocking down GPX4 expression in AGS-EBV cells. Overall design: AGS-EBV cells were transfected with lentivirus, a cell line with stable knockdown of endogenous GPX4 (AGS-EBV-shGPX4) and a control cell line (AGS-EBV-shNC) were constructed, and transcriptome sequencing was performed.