Xueli Bian

ORCID: 0000-0001-9940-8396
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About
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Research Areas
  • Ferroptosis and cancer prognosis
  • RNA modifications and cancer
  • Cancer, Lipids, and Metabolism
  • Cancer, Hypoxia, and Metabolism
  • Cancer-related gene regulation
  • Nuclear Receptors and Signaling
  • Metabolism, Diabetes, and Cancer
  • Mitochondrial Function and Pathology
  • Adenosine and Purinergic Signaling
  • Ubiquitin and proteasome pathways
  • Macrophage Migration Inhibitory Factor
  • RNA regulation and disease
  • Autophagy in Disease and Therapy
  • Epigenetics and DNA Methylation
  • Cancer Mechanisms and Therapy
  • Biochemical and Molecular Research
  • Peroxisome Proliferator-Activated Receptors
  • Lipid metabolism and biosynthesis
  • GDF15 and Related Biomarkers
  • RNA Research and Splicing
  • Protein Tyrosine Phosphatases
  • Synthesis and Characterization of Heterocyclic Compounds
  • Extracellular vesicles in disease
  • Cholesterol and Lipid Metabolism
  • Endoplasmic Reticulum Stress and Disease

First Affiliated Hospital of Jiangxi Medical College
2024

Nanchang University
2022-2024

Qingdao University
2020-2023

Affiliated Hospital of Qingdao University
2020-2023

Xiamen University
2013-2020

Abstract Gluconeogenesis, an essential metabolic process for hepatocytes, is downregulated in hepatocellular carcinoma (HCC). Here we show that the nuclear receptor Nur77 a tumour suppressor HCC regulates gluconeogenesis. Low expression clinical samples correlates with poor prognosis, and deficiency mice promotes development. interacts phosphoenolpyruvate carboxykinase (PEPCK1), rate-limiting enzyme gluconeogenesis, to increase gluconeogenesis suppress glycolysis, resulting ATP depletion...

10.1038/ncomms14420 article EN cc-by Nature Communications 2017-02-27

The natural product auraptene can influence tumor cell proliferation and invasion, but its effect on hepatocellular carcinoma (HCC) cells is unknown. Here, we report that exert anti-tumor effects in HCC via inhibition of ferroptosis induction. Auraptene treatment induces total ROS lipid production to initiate ferroptosis. death or growth induced by be eliminated the scavenger NAC GSH inhibitor ferrostatin-1 Deferoxamine Mesylate (DFO). Mechanistically, key defense protein SLC7A11 targeted...

10.3390/antiox13081015 article EN cc-by Antioxidants 2024-08-20

The crosstalk between tumor progression and ferroptosis is largely unknown. Here, we identify malate dehydrogenase 2 (MDH2) as a key regulator of ferroptosis. MDH2 deficiency inhibits hepatocellular carcinoma (HCC) cell growth promotes sensitivity HCC cells to RSL3-induced knockdown enhances intracellular reactive oxygen species (ROS), free iron ions lipid peroxides levels, leading ferroptotic death which rescued by Ferrostatin-1 chelator Deferiprone. Importantly, inhibition caused partially...

10.20944/preprints202405.1834.v2 preprint EN 2024-06-18

Ferroptosis, a recently elucidated style of regulated cell death, has emerged as significant area investigation in cancer biology. Natural active compounds that have anti-cancer effects are promising candidates for prevention. Iberverin, natural compound derived from

10.3390/biom14111407 article EN cc-by Biomolecules 2024-11-05

Metabolic enzymes can perform non-metabolic functions and play critical roles in the regulation of a variety important cellular activities. Phosphoenolpyruvate carboxykinase 1 (PCK1), gluconeogenesis enzyme, was recently identified as an AKT-regulated protein kinase that phosphorylates INSIG1/2 to promote nuclear SREBP1-dependent lipogenesis. However, relationship this with progression non-small-cell lung carcinoma (NSCLC) is unclear. Here, we demonstrate epidermal growth factor receptor...

10.3389/fonc.2021.561247 article EN cc-by Frontiers in Oncology 2021-03-26

The crosstalk between tumor progression and ferroptosis is largely unknown. Here, we identify malate dehydrogenase 2 (MDH2) as a key regulator of ferroptosis. MDH2 deficiency inhibits the growth hepatocellular carcinoma (HCC) cells enhances their sensitivity to induced by RAS-selective lethal 3 (RSL3), compound known cause knock-down RSL3-induced intracellular reactive oxygen species, free iron ions lipid per-oxides levels, leading HCC ferroptotic cell death which rescued ferrostatin-1...

10.3390/ijms252111604 article EN International Journal of Molecular Sciences 2024-10-29

The crosstalk between tumor progression and ferroptosis is largely unknown. Here, we identify malate dehydrogenase 2 (MDH2) as a key regulator of ferroptosis. MDH2 de-ficiency inhibits hepatocellular carcinoma (HCC) cell growth promotes sensitivity HCC cells to RSL3-induced knockdown enhances intracellular reactive oxygen species (ROS), free iron ions lipid peroxides levels, leading ferroptotic death which rescued by Ferrostatin-1 chelator Deferiprone. Importantly, inhibition caused...

10.20944/preprints202405.1834.v1 preprint EN 2024-05-28
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