Zhaohui Feng

ORCID: 0000-0002-8912-6456
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About
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Research Areas
  • Cancer-related Molecular Pathways
  • Cancer, Hypoxia, and Metabolism
  • Epigenetics and DNA Methylation
  • DNA Repair Mechanisms
  • Ubiquitin and proteasome pathways
  • Cytokine Signaling Pathways and Interactions
  • MicroRNA in disease regulation
  • Regulation of Appetite and Obesity
  • Reproductive System and Pregnancy
  • Carcinogens and Genotoxicity Assessment
  • interferon and immune responses
  • PI3K/AKT/mTOR signaling in cancer
  • Cancer, Lipids, and Metabolism
  • RNA modifications and cancer
  • Microtubule and mitosis dynamics
  • Metabolism, Diabetes, and Cancer
  • Pancreatic function and diabetes
  • Cancer Research and Treatments
  • CRISPR and Genetic Engineering
  • Antioxidant Activity and Oxidative Stress
  • Autophagy in Disease and Therapy
  • RNA Research and Splicing
  • Reproductive Biology and Fertility
  • Acute Myeloid Leukemia Research
  • Biochemical Analysis and Sensing Techniques

Rutgers, The State University of New Jersey
2016-2025

Rutgers Cancer Institute of New Jersey
2015-2024

Institute of Geographic Sciences and Natural Resources Research
2024

Chinese Academy of Sciences
2024

Johnson University
2020-2023

Dana-Farber Cancer Institute
2007-2021

Harvard University
2008-2021

Boston Children's Hospital
2008-2020

Jilin University
2014-2019

Union Hospital
2019

Cell growth and proliferation requires an intricate coordination between the stimulatory signals arising from nutrients factors inhibitory intracellular extracellular stresses. Alteration of often causes cancer. In mammals, mTOR (mammalian target rapamycin) protein kinase is central node in nutrient factor signaling, p53 plays a critical role sensing genotoxic other The results presented here demonstrate that activation inhibits activity regulates its downstream targets, including autophagy,...

10.1073/pnas.0502857102 article EN Proceedings of the National Academy of Sciences 2005-05-31

Whereas cell cycle arrest, apoptosis, and senescence are traditionally thought of as the major functions tumor suppressor p53, recent studies revealed two unique for this protein: p53 regulates cellular energy metabolism antioxidant defense mechanisms. Here, we identify glutaminase 2 (GLS2) a previously uncharacterized target gene to mediate these protein. GLS2 encodes mitochondrial catalyzing hydrolysis glutamine glutamate. increases expression under both nonstressed stressed conditions. by...

10.1073/pnas.1001006107 article EN Proceedings of the National Academy of Sciences 2010-04-08

Leukemia stem cells (LSCs) are capable of limitless self-renewal and responsible for the maintenance leukemia. Because selective eradication LSCs could offer substantial therapeutic benefit, there is interest in identifying signaling pathways that control their development. We studied mouse models acute myelogenous leukemia (AML) induced either by coexpression Hoxa9 Meis1a oncogenes or fusion oncoprotein MLL-AF9. show Wnt/beta-catenin pathway required derived from hematopoietic (HSC) more...

10.1126/science.1186624 article EN Science 2010-03-25

The hypothalamus and other regions within the central nervous system (CNS) link sensing of nutrients to control metabolism feeding behavior. Here, we report that intracerebroventricular (ICV) administration long-chain fatty acid oleic markedly inhibits glucose production food intake. anorectic effect was independent leptin accompanied by a decrease in hypothalamic expression neuropeptide Y. short-chain octanoic failed reproduce metabolic effects acid, ICV coadministration inhibitors...

10.2337/diabetes.51.2.271 article EN Diabetes 2002-02-01

The insulin-like growth factor 1 (IGF-1)-AKT-mTOR pathways sense the availability of nutrients and mitogens respond by signaling for cell division. p53 pathway senses a variety stress signals which will reduce fidelity division, responds initiating cycle arrest, senescence, or apoptosis. This study explores four p53-regulated gene products, beta1 beta2 subunits AMPK, are shown first time to be regulated protein, TSC2, PTEN, IGF-BP3, each negatively regulates IGF-1-AKT-mTOR after stress....

10.1158/0008-5472.can-06-4149 article EN Cancer Research 2007-04-01

Regulation of energy metabolism is a novel function p53 in tumor suppression. Parkin (PARK2) , Parkinson disease-associated gene, potential suppressor whose expression frequently diminished tumors. Here was identified as target gene that an important mediator p53's regulating metabolism. The human and mouse genes contain functional responsive elements, increases the transcription both humans mice. contributes to glucose metabolism; deficiency activates glycolysis reduces mitochondrial...

10.1073/pnas.1113884108 article EN Proceedings of the National Academy of Sciences 2011-09-19

The tumor suppressor gene p53 is frequently mutated in cigarette smoke (CS)-related lung cancer. binding pattern of carcinogenic polycyclic aromatic hydrocarbons (PAHs) found CS coincides with the mutational cancer, and PAHs have thus been considered to be major culprits for However, compared other compounds, such as aldehydes, amount minute. Acrolein (Acr) abundant CS, it can directly adduct DNA. Acr-DNA adducts, similar PAH-DNA induce predominantly G-to-T transversions human cells. These...

10.1073/pnas.0607031103 article EN Proceedings of the National Academy of Sciences 2006-10-10

Mutations in E3 ubiquitin ligase Parkin have been linked to familial Parkinson's disease. Accumulating evidence suggests that is a tumor suppressor, but the underlying mechanism poorly understood. Here we show an for hypoxia-inducible factor 1α (HIF-1α). interacts with HIF-1α and promotes degradation through ubiquitination, which turn inhibits metastasis of breast cancer cells. downregulation cells metastasis, can be inhibited by targeting RNA interference or small-molecule inhibitor YC-1....

10.1038/s41467-017-01947-w article EN cc-by Nature Communications 2017-11-22

In common forms of obesity, hyperphagia, hyperinsulinemia, and hyperleptinemia coexist. Here, we demonstrate rapid induction insulin leptin resistance by short-term overfeeding. After 3 7 days on the assigned diet regimen, rats were tested for their biological responses to acute elevations in plasma concentrations. Severe metabolic effects both ensued after just During clamp studies, glucose production was decreased ∼70% control 28–53% overfed rats. Similarly, infusion doubled contribution...

10.2337/diabetes.50.12.2786 article EN Diabetes 2001-12-01

Energy balance and insulin action are tightly coregulated. Leptin regulates energy intake expenditure partly by modulation of the melanocortin pathway in hypothalamus. Here we demonstrate potent effects on body distribution adiposity. Conscious rats received week-long infusions either a receptor agonist, α-melanocyte-stimulating hormone (α-MSH), or antagonist, SHU9119, third cerebral ventricle while food was maintained constant each group. α-MSH decreased intra-abdominal fat markedly...

10.1172/jci12954 article EN Journal of Clinical Investigation 2001-10-01

Energy balance and insulin action are tightly coregulated. Leptin regulates energy intake expenditure partly by modulation of the melanocortin pathway in hypothalamus. Here we demonstrate potent effects on body distribution adiposity. Conscious rats received week-long infusions either a receptor agonist, α-melanocyte-stimulating hormone (α-MSH), or antagonist, SHU9119, third cerebral ventricle while food was maintained constant each group. α-MSH decreased intra-abdominal fat markedly...

10.1172/jci200112954 article EN Journal of Clinical Investigation 2001-10-01
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