Abstract
Hepatoma Research is an open access journal and focuses on all topics related to hepatoma. The following articles are especially welcome: pathogenesis, clinical examination and early diagnosis of hepatoma, complications of hepatoma, and their preventions and treatments, etc.
Highlights
C-Myc is overexpressed in the majority of colorectal cancers and is required for tumor maintenance[1,2]
One clue to the development of hepatome diagnosis and therapies directed against FUSE binding protein1 (FUBP1)-interacting repressor (FIR)/FIRΔexon2/PUF60 with small molecular weight chemicals that inhibit hepatitis B virus (HBV) closed circular DNA (cccDNA) replication
Previous studies revealed that FUBP1, FIR (PUF60)/FIRΔexon2, SAP155, and SAP130 were over expressed in hepatocellular carcinoma (HCC) tissue[18]
Summary
C-Myc is overexpressed in the majority of colorectal cancers and is required for tumor maintenance[1,2]. The far upstream element (FUSE) is a sequence required for proper expression of the human c-Myc gene. FIR induces apoptosis via c-Myc suppression, and is a suitable cancer therapy[9,10]. A splicing variant of FIR that lacks exon, FIRΔexon, failed to repress c-Myc and inhibited FIR-induced apoptosis suggesting FIRΔexon is a dominant negative of FIR in human cancers[22]. SAP155, a subunit of the essential splicing factor 3B (SF3B) subcomplex in the spliceosome, is required for proper P27Kip pre-mRNA splicing, and P27Kip arrests cells at G1[30,31]. To develop novel diagnosis and therapy for hepatoma targeting FIR (PUF60)/FIRΔexon, small molecular chemical compounds against FIRΔexon were screened among 2,3275 chemicals by natural product depository (NPDepo) array at RIKEN (Japan) to develop anti-cancer drugs[35,36,37]. Small inhibitory chemicals against FIR/FIRΔexon for hepatoma therapy will be discussed
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