Yuezhen Deng

ORCID: 0009-0009-7236-9660
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About
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Research Areas
  • Cancer-related gene regulation
  • Mechanisms of cancer metastasis
  • RNA modifications and cancer
  • Ubiquitin and proteasome pathways
  • Chromatin Remodeling and Cancer
  • Signaling Pathways in Disease
  • Peptidase Inhibition and Analysis
  • Axon Guidance and Neuronal Signaling
  • Metalloenzymes and iron-sulfur proteins
  • Cancer, Hypoxia, and Metabolism
  • Cancer Mechanisms and Therapy
  • Adenosine and Purinergic Signaling
  • Epigenetics and DNA Methylation
  • Cancer-related molecular mechanisms research
  • Macrophage Migration Inhibitory Factor
  • Wnt/β-catenin signaling in development and cancer
  • Cancer-related Molecular Pathways
  • Hippo pathway signaling and YAP/TAZ
  • Liver physiology and pathology
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Pancreatic and Hepatic Oncology Research
  • interferon and immune responses
  • MicroRNA in disease regulation
  • DNA Repair Mechanisms
  • Hedgehog Signaling Pathway Studies

Shanghai Chest Hospital
2023-2024

Shanghai Jiao Tong University
2023-2024

Central South University
2019-2023

Xiangya Hospital Central South University
2019-2023

People's Hospital of Yangzhong
2023

State Key Laboratory of Respiratory Disease
2023

Shanghai Institutes for Biological Sciences
2010-2018

Chinese Academy of Sciences
2010-2018

University of Chinese Academy of Sciences
2017-2018

Cancer Research Institute
2011

Highlights•Radioresistant cancer cells reprogram metabolic flux toward glutamine anabolism•GS promotes cellular nucleotide synthesis for efficient DNA repair•High expression of GS facilitates growth under radiation stress•GS is transcriptionally regulated by STAT5SummaryRadiation resistance a critical problem in radiotherapy cancer. Radiation kills tumor mainly through causing damage. Thus, efficiency damage repair one the most important factors that limits efficacy. Glutamine...

10.1016/j.celrep.2019.07.002 article EN cc-by-nc-nd Cell Reports 2019-07-01

Intrahepatic cholangiocarcinoma (ICC) ranks as the second most malignant type of primary liver cancer with a high degree incidence and very poor prognosis. Fat mass obesity-associated protein (FTO) functions an eraser RNA m6A modification, but its roles in ICC tumorigenesis development remain unknown. We showed here that level FTO was downregulated clinical samples cell lines expression inversely correlated CA19-9 micro-vessel density (MVD). A Kaplan-Meier survival analysis low predicted...

10.3389/fonc.2019.00369 article EN cc-by Frontiers in Oncology 2019-05-09

ARID1A is a key mammalian SWI/SNF complex subunit that mutated in 5% to 11% of lung cancers. Although recent studies have elucidated the mechanism underlying dysregulation switch/sucrose non-fermentable (SWI/SNF) complexes cancers, significance loss and its implications cancers remain poorly defined. This study investigates how affects initiation progression cancer. In genetically engineered mouse models bearing mutant Kras deficient Trp53 allele (KP), (KPA) promoted tumorigenesis. Analysis...

10.1158/0008-5472.can-21-0763 article EN Cancer Research 2022-01-05

Surgical resection is the first-line treatment for hepatocellular carcinoma (HCC) patients with well-preserved liver function. Nevertheless, rate of postoperative recurrence at 5 years as high 70%, and this gravely jeopardizes therapeutic outcome. Clearly, new approaches are needed preventing relapse deadly disease. Taking advantage a luciferase-labeled orthotopic xenograft model HCC, we examined role sorafenib, first systemic drug approved advanced HCC patients, in prevention recurrence. We...

10.1002/hep.24075 article EN Hepatology 2010-11-12

Abstract Eph receptors, the largest subfamily of transmembrane tyrosine kinase have been increasingly implicated in various physiologic and pathologic processes, roles family members during tumorigenesis recently attracted growing attention. Until now, research on EphB3 function cancer is limited to focusing tumor suppression by EphB receptors colorectal cancer. However, its other types remains poorly investigated. In this study, we explored non–small-cell lung (NSCLC). We found that...

10.1158/0008-5472.can-10-0717 article EN Cancer Research 2011-01-26

Chemerin, a known chemoattractant, participates in multiple biological events. However, its role cancer remains largely unknown.Chemerin expression was evaluated by real-time PCR, western blot and immunohistochemistry. Forced expression, RNAi, immunoprecipitation, etc. were used function mechanism study. Mouse models of extrahepatic intrahepatic metastasis employed to evaluate the therapeutic potential chemerin.Chemerin significantly downregulated hepatocellular carcinoma, associated with...

10.1038/s41416-018-0077-y article EN cc-by British Journal of Cancer 2018-04-30

N6-methyladenosine (m6A) modification has been reported as a critical regulator of gene transcript expression. Although m6A plays important roles in tumor development, its role therapeutic resistance remains unknown. In this study, we aimed to examine the expression level m6A-modification related proteins and elucidate effect m6A-related on radiation response nasopharyngeal carcinoma (NPC). Among genes that participated modification, YTHDC2, reader, was found be consistently highly expressed...

10.3389/fonc.2020.01166 article EN cc-by Frontiers in Oncology 2020-07-31

Sorafenib is a specific adenosine triphosphate–competitive RAF inhibitor used as first‐line treatment of advanced hepatocellular carcinoma (HCC). However, the responses are variable, reflecting heterogeneity disease, while resistance mechanism remains poorly understood. Here, we report that sorafenib can exacerbate disease progression in both patient‐derived xenografts and cell line–derived therapeutic effect drug inversely covaries to ratio epithelial adhesion molecule–positive cells, which...

10.1002/hep.28117 article EN cc-by Hepatology 2015-08-07

Abstract Pancreatic cancer is a highly malignant tumour of the digestive tract which difficult to diagnose and treat. Approximately 90% cases arise from ductal adenocarcinoma glandular epithelium. The morbidity mortality disease have increased significantly in recent years. Its 5‐year survival rate <1% has one worst prognoses amongst tumours. low early‐stage diagnosis, high surgical cure rate. Selenium compounds produced by selenoamino acid metabolism may promote large amount oxidative...

10.1111/jcmm.16196 article EN Journal of Cellular and Molecular Medicine 2020-12-20

Although it has been widely accepted that protein arginine methyltransferase 1 (PRMT1) is a cancer-promoting gene in various cancers, the mechanism of PRMT1 hepatocellular carcinoma (HCC) requires more exploration. This study aimed to investigate role HCC growth and metastasis.We compared expression clinicopathological characteristics using paired adjacent noncancerous liver tissues from 210 patients immunohistochemistry analyses. Cell proliferation, colony formation migration were...

10.1159/000490983 article EN cc-by-nc-nd Cellular Physiology and Biochemistry 2018-01-01

Abstract Metabolic reprogramming by oncogenic signaling is a hallmark of cancer. Hyperactivation Wnt/β-catenin has been reported in hepatocellular carcinoma (HCC). However, the mechanisms inducing hyperactivation and strategies for targeting this pathway are incompletely understood. In study, we find nucleoside diphosphate kinase 7 (NME7) to be positive regulator signaling. Upregulation NME7 positively correlated with clinical features HCC. Knockdown inhibited HCC growth vitro vivo, whereas...

10.1158/0008-5472.can-21-1020 article EN cc-by Cancer Research 2021-11-11

Inflammation and metabolic reprogramming are hallmarks of cancer.How inflammation regulates cancer metabolism remains poorly understood.In this study, we found that 3-hydroxy-3-methylglutaryl-CoA lyase (HMGCL), the enzyme catalyzes catabolism leucine promotes synthesis ketone bodies, was downregulated in lung cancer.Downregulation HMGCL associated with a larger tumor size shorter overall survival time.In functional overexpression increased content β-hydroxybutyrate (β-HB) inhibited...

10.7150/ijbs.82015 article EN cc-by-nc International Journal of Biological Sciences 2023-01-01

Pancreatic cancer is one of the most malignant diseases in world. Interferon regulator factor 2 (IRF-2), an interferon regulatory factor, has been known to act as oncogene distinct types cancer. In this study, we found that expression IRF-2 was up-regulated primary pancreatic samples and associated with tumor size, differentiation, tumor–node–metastasis stage, survival patients. cells, knockdown on inhibited cell growth liquid culture soft agar. Mechanistically, modulated cells through...

10.1007/s13277-011-0273-3 article EN Tumor Biology 2011-11-25

Tumor suppressor p53, which is activated by various stress and oncogene activation, a target for anti-cancer drug development. In this study, screening panels of protein kinase inhibitors phosphatase inhibitors, we identified 5-Iodotubercidin as strong p53 activator. purine derivative used an inhibitor kinases including adenosine kinase. We found that could cause DNA damage, verified induction breaks nuclear foci positive γH2AX TopBP1, activation Atm Chk2, S15 phosphorylation up-regulation...

10.1371/journal.pone.0062527 article EN cc-by PLoS ONE 2013-05-07

NF-κB signaling is active in more than 50% of patients with pancreatic cancer and plays an important role promoting the progression cancer. Revealing activation mechanism for treatment In this study, regulation TNFα/NF-κB by VRK2 (vaccinia-related kinase 2) was investigated. The levels protein were examined immunohistochemistry (IHC). functions using CCK8 assay, anchorage-independent EdU assay tumorigenesis assay. on investigated immunoprecipitation invitro It discovered study that...

10.7150/ijbs.66313 article EN cc-by-nc International Journal of Biological Sciences 2022-01-01

Abstract The availability of asparagine is the limitation cell growth and metastasis. Asparagine synthetase (ASNS) was an essential enzyme for endogenous products. In our study, ASNS-induced products were to maintain tumor colony formations in vitro. But mutated ASNS which defected still upregulated invasiveness, indicated that promoted invasiveness by alternative pathways. Mechanically, modulated Wnt signal transduction promoting GSK3β phosphorylation on ser9 stabilizing β-catenin complex,...

10.1038/s41419-022-05015-0 article EN cc-by Cell Death and Disease 2022-06-23
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