H
Hong Liu
Researcher at Zhejiang Normal University
Publications - 30
Citations - 1069
Hong Liu is an academic researcher from Zhejiang Normal University. The author has contributed to research in topics: Cancer & Transactivation. The author has an hindex of 14, co-authored 25 publications receiving 784 citations. Previous affiliations of Hong Liu include Zhejiang University & Temple University.
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Journal ArticleDOI
Epithelial–mesenchymal transition in colorectal cancer metastasis: A system review
TL;DR: This work focuses on the molecular network of the EMT program and its malignant phenotypes associated with metastasis in colorectal cancer (CRC), including cancer stem cells, tumor budding, circulating tumor cells and drug resistance.
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Aberrantly expressed Fra-1 by IL-6/STAT3 transactivation promotes colorectal cancer aggressiveness through epithelial–mesenchymal transition
Hong Liu,Guoping Ren,Tingyang Wang,Yuexia Chen,Chaoju Gong,Yanfeng Bai,Bo Wang,Hongyan Qi,Jing Shen,Lijun Zhu,Cheng Qian,Maode Lai,Jimin Shao +12 more
TL;DR: A novel mechanism of the inflammatory cytokine IL-6 induced Fra-1 upregulation through activating STAT3 by phosphorylation and acetylation is described, demonstrating that this signaling pathway plays a critical role in promoting epithelial–mesenchymal transition and aggressiveness of colorectal cancer.
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Adenovirus type 2 activates cell cycle-dependent genes that are a subset of those activated by serum.
Hong Liu,R Baserga,W E Mercer +2 more
TL;DR: The data suggest that the mechanisms by which serum and adenovirus induce cellular DNA synthesis are not identical, and it is concluded that the cell cycle-dependent genes activated by adanovirus 2 are a subset of the cell Cycle-dependent gene activated by serum.
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Expression of thymidine kinase and dihydrofolate reductase genes in mammalian ts mutants of the cell cycle.
TL;DR: It is concluded that the expression of different genes is affected differently by the ts block in G1, even when these genes are all growth-related, even though the cells are blocked in the G1 phase.
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IL-13/STAT6 signaling plays a critical role in the epithelial-mesenchymal transition of colorectal cancer cells
TL;DR: It is shown that the pleiotropic cytokine interleukin-13 (IL-13) could induce an aggressive phenotype displaying EMT by enhancing the expression of EMT-promoting factor ZEB1 and the STAT6 signaling inhibitor and STAT6 knockdown significantly reversed IL-13-induced EMT and Z EB1 induction in CRC cells.