Computational Discovery of Niclosamide Ethanolamine, a Repurposed Drug Candidate That Reduces Growth of Hepatocellular Carcinoma Cells In Vitro and in Mice by Inhibiting Cell Division Cycle 37 Signaling.
Mucin1 mediates autocrine transforming growth factor beta signaling through activating the c-Jun N-terminal kinase/activator protein 1 pathway in human hepatocellular carcinoma cells.
Among them, one novel SNP was found in activator protein-1 (AP2), a transcription factor binding site (-483 A to C) that may be associated with the susceptibility to HCC (P = 0.012) but no associations were found for other observed variations.This mutation could be tumor-specific.
Our analysis indicated that several differentially co-express genes might play crucial roles in HCC development, including NA3C2, AHR, MYC, FOXO1 and FOSB.
We evaluated the expression of KITENIN and AP-1 target genes at mRNA levels by RT-PCR in human HCC tissues and paired normal hepatic mucosa of the same patients taken by surgery.
Our results reveal a new AP-1 site within the TRAIL promoter functionally involved in TGF-beta-induced TRAIL expression and apoptosis in hepatomas and thus provide evidence for the underlying mechanism by which TGF-beta might regulate cell death in liver cancer.
In conclusion, our findings demonstrated for the first time that acetaldehyde activated NF-kappaB and AP-1 activities via IkappaB, JNK/beta-TrCP, and p38 signaling pathways, resulting in MMP-9 gene expression and hepatocarcinoma cells invasion.