H
Huadan Xu
Researcher at Jilin University
Publications - 8
Citations - 118
Huadan Xu is an academic researcher from Jilin University. The author has contributed to research in topics: Warburg effect & Apoptosis. The author has an hindex of 4, co-authored 7 publications receiving 63 citations.
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Journal ArticleDOI
Dicumarol inhibits PDK1 and targets multiple malignant behaviors of ovarian cancer cells.
Wenjia Zhang,Jing Su,Huadan Xu,Shanshan Yu,Yanan Liu,Yong Zhang,Liankun Sun,Ying Yue,Xiaoli Zhou +8 more
TL;DR: DIC potently inhibited the kinase activity of PDK1, shifted the glucose metabolism from aerobic glycolysis to oxidative phosphorylation, generated a higher level of reactive oxygen species (ROS), attenuated the mitochondrial membrane potential (MMP), induced apoptosis, and reduced cell viability in vitro.
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Deficiency in IL-33/ST2 Axis Reshapes Mitochondrial Metabolism in Lipopolysaccharide-Stimulated Macrophages.
TL;DR: The findings suggested that the pleiotropic IL-33/ST2 pathway may influence the polarization and function of macrophages by regulating mitochondrial metabolism.
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PGC1α promotes cisplatin resistance in human ovarian carcinoma cells through upregulation of mitochondrial biogenesis
TL;DR: Evidence is provided that cisplatin stimulated the expression of P GC1α and the upregulation of mitochondrial biogenesis through PGC1α, promoting cell viability and inhibiting apoptosis in response to cisplin treatment, thus triggering cis platin resistance in ovarian cancer cells.
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The IL-33/ST2 axis affects tumor growth by regulating mitophagy in macrophages and reprogramming their polarization.
TL;DR: The IL-33/ST2 axis was demonstrated to play an important role in the metabolic conversion of macrophages from OXPHOS to glycolysis by altering mitophagy levels, and promoted enhanced cell oxidative phosphorylation, thereby further increasing M2 polarization gene expression and ultimately promoting tumor growth.
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Regulation of Integrated Stress Response Sensitizes U87MG Glioblastoma Cells to Temozolomide Through the Mitochondrial Apoptosis Pathway.
TL;DR: It is suggested that ISR and ATF4 are involved in the death crosstalk between the endoplasmic reticulum and mitochondria and might be a potential target to enhance the therapeutic effect of temozolomide in patients with glioblastoma multiforme.