J
Jinming Shi
Researcher at Northeast Forestry University
Publications - 23
Citations - 337
Jinming Shi is an academic researcher from Northeast Forestry University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 7, co-authored 16 publications receiving 210 citations.
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Journal ArticleDOI
In vivo anti-radiation activities of the Ulva pertusa polysaccharides and polysaccharide–iron(III) complex
TL;DR: Results proved that the anti-radiation and anti-oxidative activity of iron(III) complex of low molecular-weight polysaccharides were not less than that of low Molecular-weight Polysaccharide with low molecular weight.
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The role of YY1 in oncogenesis and its potential as a drug target in cancer therapies.
TL;DR: Based on the expression feature and regulatory activities in tumor cells, YY1 possesses a great potential as a biomarker for many cancers and can serve as a therapeutic target clinically to impede cancer development and progression or sensitize cancer cells to anticancer drugs.
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Fatty acid synthase is a primary target of MiR-15a and MiR-16-1 in breast cancer.
Jingxuan Wang,Xiao Zhang,Jinming Shi,Paul Cao,Meimei Wan,Qiang Zhang,Yunxuan Wang,Steven J. Kridel,Wennuan Liu,Jianfeng Xu,Qingyuan Zhang,Guangchao Sui +11 more
TL;DR: It is demonstrated that FASN expression is primarily downregulated by miR-15a and mi-16-1 in mammary cells and FASn is one of the major targets of these two tumor suppressive microRNAs.
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Ellagic acid synergistically potentiates inhibitory activities of chemotherapeutic agents to human hepatocellular carcinoma.
TL;DR: It is discovered that EA synergistically potentiated DOX and DDP in suppressing HCC with significantly reduced side effects and this may represent a novel strategy in HCC therapies with both high anticancer efficiencies and low systemic toxicity in patients.
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Yin Yang 1 promotes mTORC2-mediated AKT phosphorylation
Qiang Zhang,Meimei Wan,Jinming Shi,David A. Horita,Lance D. Miller,Timothy E. Kute,Steven J. Kridel,George Kulik,Guangchao Sui +8 more
TL;DR: It is demonstrated for the first time that YY 1 promotes mTORC2-mediated AKT activation and disrupting YY1-AKT interaction by OPB domain-based peptide may represent a potential strategy for cancer therapy.