C. Zeng

Publications5
h-index3
Citations23
Highly Influential Citations1
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Overexpression of EPS8L3 promotes cell proliferation by inhibiting the transactivity of FOXO1 in HCC.
TLDR
Experiments illustrated that overexpressing EPS8L3 promotes the expression of p-AKT, Cyclin D1, but inhibits the transcriptional activity of FOXO1, and suggested that EPS8l3 may be a novel therapeutic target for HCC.
TCF19 enhances cell proliferation in hepatocellular carcinoma by activating the ATK/FOXO1 signaling pathway.
TLDR
The combined results suggest that crucial links between TCF19 and HCC can provide a novel target for hepatocellular carcinoma treatment.
Nicotine promotes WRL68 cells proliferation due to the mutant p53 gain-of-function by activating CDK6-p53-RS-PIN1-STAT1 signaling pathway.
TLDR
Chronic exposure to nicotine significantly promotes human normal fetal hepatic cell line (WRL68 cells) proliferation in a time- and concentration-dependent manner resulting from G0/G1-S-phase transition and indicates that nicotine induces mutant p53 gain-of function (GOF), activating CDK6-p53-RS-PIN1-STAT1 signaling pathway and promoting cell proliferation, which could contribute to HCC for smokers.
p53 Mutation at Serine 249 and Its Gain of Function Are Highly Related to Hepatocellular Carcinoma after Smoking Exposure
TLDR
It strongly demonstrated that tobacco smoking is positively and independently associated with HCC, which may be attributed to p53-RS and its gain of function.
Tobacco Smoking is Positively Associated with Hepatocellular Carcinoma Due to the p53 Mutation at Serine 249
TLDR
It was demonstrated that tobacco smoking is positively and independently associated with HCC, which may be attributed to p53-RS and its gain of function.