Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A library of cell-permeable, minimally tagged C75 analogues was synthesized and used to uncover biological targets in human liver cancer cells. Known targets of C75, namely FASN and CPT1A, together with other unknown targets, including PDIA3, TFRC, and GAPDH, were thus identified.
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PMID:In situ proteome profiling of C75, a covalent bioactive compound with potential anticancer activities. 2455 42

Iron metabolism is crucial to hepatocellular carcinoma progression and is a key determinant of prognosis. Protein-protein interactions within the iron metabolism gene network were analyzed using the European Molecular Biology Laboratory's Search Tool for Recurring Instances of Neighbouring Genes/Proteins database. We obtained 423 liver hepatocellular carcinoma gene expression profiles from the Cancer Genome Atlas database. The expression and pathway enrichment of representative iron intake genes (TFRC and DMT1), utilization genes (FTH1, FTL, HIF1A, HMOX1, SLC25A37, and SLC25A38), and efflux genes (FLVCR1 and SLC40A1) was investigated in tumor and adjacent tissues. We determined the relationship between iron metabolism and the prognostic features of liver hepatocellular carcinoma. The liver metabolism genes TFRC and FLVCR1 were related to survival, disease status, and prognosis in patients with hepatocellular carcinoma. Our results provide novel insight into liver cancer therapy.
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PMID:Iron metabolism gene expression and prognostic features of hepatocellular carcinoma. 3007 42

Estrogen (E2) regulates hundreds of genes involved in cell metabolism and disrupts iron homoeostasis in various cell types. Herein, we addressed whether E2-induced epigenetic modifications are involved in modulating the expression of iron-regulatory genes. Epigenetic status of FTH1 and TFRC genes was assessed in E2-treated cancer cells. E2-induced DNA methylation was associated with decreased FTH1 and TFRC expression in Hep-G2 and Huh7 cells, but not in AGS or MCF7 cells. Demethylation with 5-Aza-2-deoxycytidine upregulated the expression of both these genes in Hep-G2 cells. The expression of DNMT3B, PRMT5, and H4R3me2s increased in E2-treated cells. Chromatin immunoprecipitation showed that E2 treatment recruited PRMT5 and H4R3me2s on FTH1 but not on TFRC. Knockdown of PRMT5, DNMT3B, and Estrogen-receptor alpha rescued FTH1 from E2-induced silencing. However, knockdown of DNMT3B alone blocked the inhibitory effects of E2 on TFRC. Analysis of human liver tissues in publicly available datasets showed that FTH1 and TFRC are highly expressed in primary liver tumours, but a lower expression is associated with better survival. Interestingly, we showed that the silencing of FTH1 and/or TFRC inhibited carcinogenesis in Hep-G2 cells. For the first time, our findings uncovered the novel signalling pathway involved in the protective effects of E2 against liver cancer.
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PMID:Estrogen-induced epigenetic silencing of FTH1 and TFRC genes reduces liver cancer cell growth and survival. 3247 55