Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From a metabolic perspective, cancer may be considered as a metabolic disease characterized by reprogrammed glycolytic metabolism. The aim of the present study was to investigate CD147-mediated glucose metabolic regulation in hepatocellular carcinoma (HCC) and its contribution to altered immune responses in the tumor microenvironment. Several HCC cell lines and corresponding nude mice xenografts models differing in CD147 expressions were established to directly investigate the role of CD147 in the reprogramming of glucose metabolism, and to determine the underlying molecular mechanisms. Immunohistochemistry (IHC) analyses and flow cytometry were used to identify the relationship between reprogrammed glycolysis and immunosuppression in HCC. Upregulated CD147 expressions were found to be associated with enhanced expressions of GLUT1, MCT1 in HCC tumorous tissues. CD147 promoted the glycolytic metabolism in HCC cell lines in vitro via the PI3K/Akt/mTOR signaling pathway. A positive correlation existed between a profile of immunosuppressive lymphocytes infiltration and CD147 expression in HCC tissues. Accumulation of FOXP3-expressing regulatory T cells was induced under a stimulation with lactate in vitro. In conclusion, CD147 promoted glycolytic metabolism in HCC via the PI3K/Akt/mTOR signaling pathway, and was related to immunosuppression in HCC.
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PMID:Enhanced glucose metabolism mediated by CD147 contributes to immunosuppression in hepatocellular carcinoma. 3196 68

It is reported that long noncoding RNA RHPN1-AS1 (lncRNA RHPN1-AS1) functions as an oncogene among multiple types of cancers; however, the effect of lncRNA RHPN1-AS1 in hepatocellular carcinoma (HCC) is left to be investigated. The main purpose of this work was to study the effects of lncRNA RHPN1-AS1/miR-485-5p system on proliferation, migration, and invasion in HCC and future investigate the latent mechanisms. Our work found that lncRNA RHPN1-AS1 was observably up-regulated in HCC tissues and cell lines, especially HCCLM3 and SMMC-7721 cells. LncRNA RHPN1-AS1 knockdown decreased the capacity of proliferation, invasion, and migration in HCCLM3 and SMMC-7721 cells, which could be crippled by miR-485-5p inhibitor. Besides, the expression of basigin (BSG) was decreased after lncRNA RHPN1-AS1 silence, indicating the function of lncRNA RHPN1-AS1/miR-485-5p/BSG axis in HCC progression. Our study opens novel insights to help understand the mechanisms of lncRNA RHPN1-AS1/miR-485-5p/BSG axis in HCC progression, which may provide a new therapeutic target for HCC treatment.
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PMID:LncRNA RHPN1-AS1 accelerates proliferation, migration, and invasion via regulating miR-485-5p/BSG axis in hepatocellular carcinoma. 3243 75

Chimeric antigen receptor (CAR) therapy is a promising immunotherapeutic strategy for treating multiple refractory blood cancers, but further advances are required for solid tumor CAR therapy. One challenge is identifying a safe and effective tumor antigen. Here, we devise a strategy for targeting hepatocellular carcinoma (HCC, one of the deadliest malignancies). We report that T and NK cells transduced with a CAR that recognizes the surface marker, CD147, also known as Basigin, can effectively kill various malignant HCC cell lines in vitro, and HCC tumors in xenograft and patient-derived xenograft mouse models. To minimize any on-target/off-tumor toxicity, we use logic-gated (log) GPC3-synNotch-inducible CD147-CAR to target HCC. LogCD147-CAR selectively kills dual antigen (GPC3+CD147+), but not single antigen (GPC3-CD147+) positive HCC cells and does not cause severe on-target/off-tumor toxicity in a human CD147 transgenic mouse model. In conclusion, these findings support the therapeutic potential of CD147-CAR-modified immune cells for HCC patients.
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PMID:Efficacy of anti-CD147 chimeric antigen receptors targeting hepatocellular carcinoma. 3296 61


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