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)

Many trials using DNA microarrays have been reported for various human malignancies, but an efficient molecular diagnostic system has yet to be established. Here, we adopted a high throughput quantitative PCR-array system based on adaptor-tagged competitive PCR (ATAC-PCR), as a novel technique for gene expression profiling of hepatocellular carcinoma (HCC). This PCR-array contained 3,072 genes derived from three different cDNA libraries, including 298 additional known genes suspected to be involved in hepatocarcinogenesis. Using this PCR-array with 20 pairs of liver tissues (20 HCC, 20 surrounding nontumor liver), we identified a total of 117 genes differing in expression levels in the two liver tissues. Hierarchical clustering analysis and principal component analysis with these genes revealed distinct gene expression patterns in the HBV-positive group and the HCV-positive groups. Among 117 genes, only 7 (GPAA1, TMEM9, FACL4, ADFP, MAWBP, PACE4, FOS) were common to both groups. In conclusion, this PCR-array analysis with an appropriate set of genes is considered useful for gene expression profiling of HCC, and we identified some genes which may play a common key role in hepatocarcinogenesis.
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PMID:PCR-array gene expression profiling of hepatocellular carcinoma. 1514 62

Although it is known that Phenazine biosynthesis-like domain-containing protein (PBLD) expression is downregulated in hepatocellular carcinoma (HCC), its biological function is unclear. Additionally, no agents capable of upregulating PBLD exist. In the current study, the relationship between PBLD and HCC was analyzed using clinicopathological specimens. A HCC cell model, microarray analysis and an animal model were used to verify the therapeutic effect of cedrelone on HCC. The present study demonstrated that PBLD inhibited HCC progression. Furthermore, the present study revealed that cedrelone possessed treated-HCC capabilities via targeted PBLD overexpression. The epithelial-mesenchymal transition phenotype and growth rate were inhibited and the apoptosis ratio was promoted by cedrelone following PBLD overexpression. The Ras and Ras-proximate-1 signaling pathways were also determined to be regulated by cedrelone via PBLD activation in HCC. PBLD may therefore be an independent predictor of HCC progression and a novel target for HCC treatment. Additionally, the PBLD activator, cedrelone, may be a potential drug for HCC treatment in the future.
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PMID:Novel compound cedrelone inhibits hepatocellular carcinoma progression via PBLD and Ras/Rap1. 3177 31