Guoliang Liu

Publications (2)9.58 Total impact

• Article: GRIM-19 Opposes Reprogramming of Glioblastoma Cell Metabolism via HIF1α Destabilization.

  Qian Liu, Lulu Wang, Zhaojuan Wang, Yang Yang, Jingxia Tian, Guoliang Liu, Dongshi Guan, Xinmin Cao, Yanmin Zhang, Aijun Hao
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  ABSTRACT: The metabolism that sustains cancer cells is adapted preferentially to glycolysis, even under aerobic conditions (Warburg effect). This effect was one of the first alterations in cancer cells recognized as conferring a survival advantage. Here, we show that Genes Associated with Retinoid-interferon-induced Mortality 19 (GRIM-19), which was previously identified as a tumor suppressor protein associated with growth inhibition and cell apoptosis, contributes to the switch between oxidative and glycolytic pathways. In parallel to this, vascular endothelial growth factor (VEGF) which promotes neovascularization is also regulated. We have identified hypoxia inducible factor 1α (HIF1α) as the downstream factor of GRIM-19 in human glioblastoma cell lines. Down-regulation of GRIM-19 promotes HIF-1α synthesis in a STAT3 dependent manner, which acts as a potential competitive inhibitor for von Hippel-Lindau (pVHL)-HIF1α interaction, and thereby prevents HIF1α from pVHL-mediated ubiquitination and proteasomal degradation. Taken together, it is concluded that GRIM-19, a potential tumor suppressor gene, performs its function in part via regulating glioblastoma metabolic reprogramming through STAT3-HIF1α signaling axis, and this has added new perspective to its role in tumorigenesis thus providing potential strategies for tumor metabolic therapy.
  Carcinogenesis 04/2013; · 5.70 Impact Factor
• Article: Depletion of GRIM-19 accelerates hepatocellular carcinoma invasion via inducing EMT and loss of contact inhibition.

  Hongbo Hao, Jun Liu, Guoliang Liu, Dongshi Guan, Yang Yang, Xiuqing Zhang, Xinmin Cao, Qian Liu
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  ABSTRACT: Genes associated with retinoid-interferon-induced mortality 19 (GRIM-19) was identified as a tumor suppressor protein associated with apoptosis and growth inhibition. Here, we report that the expression levels of GRIM-19 are significantly attenuated in hepatocellular carcinoma (HCC) patients with deteriorating differentiation states, hepatic capsule invasion and microvascular invasion, suggesting the potential role of GRIM-19 not only at the origin but also in the invasive progression of HCCs. To dissect the possible mechanisms by which GRIM-19 regulates tumor cell invasion, we established the hepatic HL-7702 and HCC Huh-7 cell lines stably depleted of GRIM-19. Results show that downregulation of GRIM-19 induces a morphological transformation resembling epithelial-mesenchymal transition (EMT) as well as aberrant expression of epithelial and mesenchymal molecular markers. Additionally, these cells lose contact inhibition, a phenomenon of cessation of cell migration in contact with neighboring cells, as assessed by cell imaging, growth curve and S-phase transition in confluent conditions. CONCLUSION: Our observations demonstrate a novel mechanistic insight into a critical role of GRIM-19 in HCC invasive potential.
  Journal of Cellular Physiology 11/2011; 227(3):1212-9. · 3.87 Impact Factor