Yongmei Li
Tianjin Medical University
20 Papers
32 Citations
Yongmei Li is an academic researcher from Tianjin Medical University. The author has contributed to research in topics: Metastasis & Medicine. The author has an hindex of 12, co-authored 16 publications. Previous affiliations of Yongmei Li include Tianjin Medical University Cancer Institute and Hospital.
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Papers
Quantitative proteomics reveals that long non-coding RNA MALAT1 interacts with DBC1 to regulate p53 acetylation.
Ruibing Chen,Yun Liu,Hao Zhuang,Hao Zhuang,Baicai Yang,Kaiwen Hei,Mingming Xiao,Chunyu Hou,Huajun Gao,Xinran Zhang,Chenxi Jia,Chenxi Jia,Lingjun Li,Lingjun Li,Yongmei Li,Ning Zhang +15 more
TL;DR: A novel mechanism by which MALAT1 regulates the activity of p53 through the lncRNA–protein interaction is uncovered by combining RNA pull-down, quantitative proteomics, bioinformatics, and experimental validation.
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Interactome analysis reveals that lncRNA HULC promotes aerobic glycolysis through LDHA and PKM2
Chunqing Wang,Yongmei Li,Shuai Yan,Hao Wang,Hao Wang,Xianfeng Shao,Mingming Xiao,Baicai Yang,Guoxuan Qin,Ruirui Kong,Ruibing Chen,Ning Zhang,Ning Zhang +12 more
TL;DR: A quantitative proteomics strategy to identify long noncoding RNA (lncRNA)-binding proteins in vivo is presented and its application is demonstrated by characterizing the lncRNA HULC, which is shown to interact with glycolytic enzymes and modulate their activity.
cPLA2α activates PI3K/AKT and inhibits Smad2/3 during epithelial-mesenchymal transition of hepatocellular carcinoma cells.
TL;DR: The data suggested that cPLA2α mediate epidermal growth factor (EGF) induced epithelial-mesenchymal transition (EMT) through PI3K/AKT/ERK pathway and is a potentially target for novel therapies of HCC.
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Glycine decarboxylase induces autophagy and is downregulated by miRNA-30d-5p in hepatocellular carcinoma.
TL;DR: It is shown that a high GLDC expression level is associated with better overall survival and is an independent factor for the favorable prognosis of HCC patients, and suggests that GLDC may play an important role to increasing miR-30d-5p-reduced autophagy to suppress HCC progress.
Demethylation-Induced Overexpression of Shc3 Drives c-Raf-Independent Activation of MEK/ERK in HCC.
Yun Liu,Xinran Zhang,Baicai Yang,Hao Zhuang,Hao Zhuang,Guo Hua,Wen Wei,Yuan Li,Ruibing Chen,Yongmei Li,Ning Zhang +10 more
TL;DR: Ectopic expression of Shc3 forms a complex with MVP/MEK/ERK to potentiate ERK activation and plays an important role in sorafinib resistance in HCC.