H
Hui Lin
Researcher at Nanchang University
Publications - 18
Citations - 408
Hui Lin is an academic researcher from Nanchang University. The author has contributed to research in topics: AMPK & Metformin. The author has an hindex of 9, co-authored 18 publications receiving 253 citations. Previous affiliations of Hui Lin include Boston University.
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Journal ArticleDOI
AMPK Inhibits the Stimulatory Effects of TGF-β on Smad2/3 Activity, Cell Migration, and Epithelial-to-Mesenchymal Transition.
Hui Lin,Nianshuang Li,Huan He,Ying Ying,Shashank Sunkara,Lingyu Luo,Nonghua Lv,Deqiang Huang,Zhijun Luo +8 more
TL;DR: The results showed that activation of AMPK by metformin inhibited TGF-β–induced Smad2/3 phosphorylation in cancer cells in a dose-dependent manner, and suggested that AMPK could be a drug target for controlling cancer progression and metastasis.
Journal ArticleDOI
LKB1/AMPK inhibits TGF-β1 production and the TGF-β signaling pathway in breast cancer cells
Nianshuang Li,Junrong Zou,Hui Lin,Hui Lin,Rong Ke,Xiaoling He,Lu Xiao,Deqiang Huang,Lingyu Luo,Nonghua Lv,Zhijun Luo,Zhijun Luo +11 more
TL;DR: It is suggested that AMPK inhibits the transcription of TGF-β1, leading to reduction of its concentration in serum, and metformin suppressed epithelial-to-mesenchymal transition of mammary epithelial cells.
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Metformin, an Old Drug, Brings a New Era to Cancer Therapy
TL;DR: This review summarizes recent progress in studies of metformin use in cancer and discusses the possibility to enhance its efficacy and to prevent cancer metastasis.
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Inonotus obliquus polysaccharides induces apoptosis of lung cancer cells and alters energy metabolism via the LKB1/AMPK axis.
TL;DR: The results demonstrate that IOP acts on cancer cells through a mechanism by which AMPK triggers the apoptotic pathway via the opening of mitochondrial permeability transition pore, and reducing MMP, leading to an inhibition of ATP production.
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Metformin induces ferroptosis by targeting miR-324-3p/GPX4 axis in breast cancer.
TL;DR: In this article, the effect of metformin on breast cancer was explored and the underlying mechanism of the mechanism was clarified. But, the results showed that the effect was mediated by directly targeting glutathione peroxidase 4 (GPX4) and led to downregulation of GPX4.