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Hepatitis B virus X (HBX) protein upregulates β-catenin in a human hepatic cell line by sequestering SIRT1 deacetylase.
TLDR
It is proposed that HBX upregulates β-catenin by sequestering SIRT1, which leads to anticancer drug resistance and could be a therapeutic strategy for HBV-related hepatocellular carcinoma.
SIRT1 sensitizes hepatocellular carcinoma cells expressing hepatitis B virus X protein to oxidative stress-induced apoptosis.
TLDR
Results suggest that up-regulation of SIRT1 under oxidative stress may be a therapeutic strategy for treatment of hepatocellular carcinoma cells related to HBV through inhibition of JNK activation.
Up-regulation of Foxo4 mediated by hepatitis B virus X protein confers resistance to oxidative stress-induced cell death.
TLDR
It is shown that HBX induces the up-regulation of Forkhead box class O 4 (Foxo4) not only in Chang cells stably expressing HBX (Chang-HBX) but also in primary hepatic tissues from HBX-transgenic mice, and it is proposed that Foxo4 may be a useful target for suppression in the treatment of HBV-associated hepatocellular carcinoma cells.
CUG2, a novel oncogene confers reoviral replication through Ras and p38 signaling pathway
TLDR
It is proposed that reovirus can be useful in the treatment of transformed cells expressing CUG2, which is commonly detected in various tumor tissues.
Inhibition of GSK-3beta enhances reovirus-induced apoptosis in colon cancer cells.
TLDR
It is proposed that inhibition of GSK-3beta sensitizes reovirus-induced apoptosis of colon cancer cells by down-regulation of NF-kappaB activity, offering a potentially improved therapeutic strategy for the treatment of Colon cancer.
Cancer upregulated gene 2, a novel oncogene, confers resistance to oncolytic vesicular stomatitis virus through STAT1-OASL2 signaling
TLDR
It is proposed that VSV treatment combined with the selective regulation of genes such as STAT1 and OASL2 will improve therapeutic outcomes for CUG2-overexpressing tumors.
Suppression of autophagic genes sensitizes CUG2-overexpressing A549 human lung cancer cells to oncolytic vesicular stomatitis virus-induced apoptosis.
TLDR
It is proposed that autophagy impairment is a potential strategy for successful VSV virotherapy of CUG2-overexpressing tumors because it induces excessive ROS formation, which decreases S6 kinase activity and ISG15 expression, ultimately rendering the A549-CUG2 cells susceptible to VSV infection.
SIRT1 inhibits proliferation of pancreatic cancer cells expressing pancreatic adenocarcinoma up-regulated factor (PAUF), a novel oncogene, by suppression of β-catenin.
TLDR
Results suggest that SIRT1 activation may be a therapeutic strategy for treatment of pancreatic cancer cells that express PAUF via the down-regulation of β-catenin.
Hepatitis B virus X protein inhibits extracellular IFN-α-mediated signal transduction by downregulation of type I IFN receptor
TLDR
It is proposed that HBX downregulates IFNAR1, leading to the avoidance of extracellular IFN-α signal transduction, and is also proposed that Tyk2, which is required for the stable expression of IFnAR1 on the cell surface, is downregulated.
Cancer upregulated gene 2, a novel oncogene, enhances migration and drug resistance of colon cancer cells via STAT1 activation.
TLDR
The results suggest that CUG2 enhances metastasis and drug resistance through STAT1 activation, which eventually contributes to tumor progression.
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