fig5

Novel diagnosis and therapy for hepatoma targeting HBV-related carcinogenesis through alternative splicing of FIR (PUF60)/FIRΔexon2

Figure 5. BK697 inhibit far upstream element-binding protein-interacting repressor Δexon2 (FIRΔexon2) that is considered as a dominant negative of FIR. (A) From computer screening to search synthesized chemicals that mimicking the structure of the identified compound using Namiki database (Namiki Shoji Co., Ltd., Tokyo, Japan) that was composed of commercially available chemicals after natural product depository array at RIKEN (Japan). Affiliated chemicals were screened and indicated in the square (square). Based on the computer screening, lots of similar chemicals were designed and seven compounds were selected for treating with HLE and HLF cells to examine cell growth inhibition (arrows); (B) BK697 effectively suppressed hepatoblastoma cells, HLE and HLF cells. BK697 effectively suppressed hepatoblastoma cells, HLE and HLF cells by MTS assay (see materials and methods). Small molecular weight indicated arrows (A) were examined the cell growth suppression in HLE and HLF cells. All samples are tested in duplicate, absorbencies were tested 3 times. Same volume of DMSO was used as negative control. Same volume of 3% H2O2 was used as positive control; (C) BK697 suppressed FIR/FIRΔexon2 expression on dose-dependent manner in gastric cancer cells (left) and HeLa cells (right). Note SAP155 (SF3B1) was also suppressed by BK697 along with FIR/FIRΔexon2 expression. H2AX is a marker of DNA damage. FIR: FUBP1-interacting repressor; HLE: hepatoblastoma cell line; MTS: 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt; DMSO: dimethyl sulfoxide

Hepatoma Research
ISSN 2454-2520 (Online) 2394-5079 (Print)

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