- Ubiquitin and proteasome pathways
- RNA modifications and cancer
- Ferroptosis and cancer prognosis
- Autophagy in Disease and Therapy
- Peptidase Inhibition and Analysis
- Endoplasmic Reticulum Stress and Disease
- Heme Oxygenase-1 and Carbon Monoxide
- Cancer, Hypoxia, and Metabolism
- Cancer-related gene regulation
- Cancer-related molecular mechanisms research
- Neonatal Health and Biochemistry
- Cancer-related Molecular Pathways
- Mitochondrial Function and Pathology
- Histone Deacetylase Inhibitors Research
- Immune cells in cancer
- Cancer, Lipids, and Metabolism
- Medical Research and Treatments
- Thyroid Disorders and Treatments
- Epigenetics and DNA Methylation
- Multiple Myeloma Research and Treatments
- Higher Education and Teaching Methods
- Growth Hormone and Insulin-like Growth Factors
- Chronic Myeloid Leukemia Treatments
- Neonatal Respiratory Health Research
- Extracellular vesicles in disease
Guangzhou Medical University
2016-2025
State Key Laboratory of Respiratory Disease
2003-2025
China University of Mining and Technology
2024
Shandong University of Traditional Chinese Medicine
2024
Third Affiliated Hospital of Guangzhou Medical University
2017-2022
Xi'an University of Technology
2020-2022
Shaanxi Provincial Land Engineering Construction Group
2020-2022
China Land Surveying and Planning Institute
2020
University of South Dakota
2020
Hebei North University
2009-2011
Ferroptosis is a form of regulated cell death that may facilitate the selective elimination tumor cells. The suppressor p53 (TP53) has been demonstrated to promote ferroptosis via transcription-dependent mechanism. Here, we show TP53 limits erastin-induced by blocking dipeptidyl-peptidase-4 (DPP4) activity in transcription-independent manner. Loss prevents nuclear accumulation DPP4 and thus facilitates plasma-membrane-associated DPP4-dependent lipid peroxidation, which finally results...
Ferroptosis is a type of iron-dependent regulated cell death characterized by unrestricted lipid peroxidation and membrane damage. Although GPX4 (glutathione peroxidase 4) plays master role in blocking ferroptosis eliminating phospholipid hydroperoxides, the regulation remains poorly understood. Here, we report an unexpected for copper promoting ferroptotic death, but not cuproptosis, inducing macroautophagic/autophagic degradation GPX4. Copper chelators reduce sensitivity do inhibit other...
Selective macroautophagy/autophagy maintains cellular homeostasis through the lysosomal degradation of specific proteins or organelles. The pro-survival effect selective autophagy has been well-characterized, but mechanism by which it drives cell death is still poorly understood. Here, we use a quantitative proteomic approach to identify HPCAL1 (hippocalcin like 1) as novel receptor for CDH2 (cadherin 2) during ferroptosis. HPCAL1-dependent depletion increases susceptibility ferroptotic...
Posttranslational modifications add tremendous complexity to proteomes; however, gaps remain in knowledge regarding the function and regulatory mechanism of newly discovered lysine acylation modifications. Here, we compared a panel non-histone patterns metastasis models clinical samples, focused on 2-hydroxyisobutyrylation (Khib) due its significant upregulation cancer metastases. By integration systemic Khib proteome profiling 20 paired primary esophageal tumor metastatic tissues with...
Abstract Ferroptosis is a type of lipid peroxidation-dependent cell death that emerging as therapeutic target for cancer. However, the mechanisms ferroptosis during generation and detoxification peroxidation products remain rather poorly defined. Here, we report an unexpected role eukaryotic translation initiation factor EIF4E determinant ferroptotic sensitivity by controlling peroxidation. A drug screening identified 4EGI-1 4E1RCat (previously known EIF4E-EIF4G1 interaction inhibitors)...
Abstract Dysregulation of the ubiquitin‐proteasome pathway plays an essential role in tumor growth and development. Shikonin, a natural naphthoquinone isolated from traditional Chinese medicine Zi Cao ( gromwell ), has been reported to possess cell‐killing activity, results clinical study using shikonin‐containing mixture demonstrated its safety efficacy for treatment late‐stage lung cancer. In this study, we that shikonin is inhibitor proteasome activity vitro vivo . Our computational...
Proteasomal deubiquitinase (DUB) inhibition has been found to be effective in experimental cancer therapy by inducing proteasome and apoptosis. Ferroptosis is a form of regulated cell death characterized an iron-dependent lipid peroxidation. Antioxidant enzyme glutathione peroxidase 4 (GPX4) plays key role blocking ferroptosis through directly reducing phospholipid hydroperoxides production. Since cytoplasmic DUB can promote protein degradation the cell, we hypothesize that induces GPX4...
Long noncoding RNAs (lncRNA) have been observed in various cancer types. Our bioinformatic analysis of existing databases demonstrated overexpression lncRNA THAP9-AS1 pancreatic ductal adenocarcinoma (PDAC). We aimed to investigate the roles and mechanisms PDAC.The samples patients with was characterized associated clinical outcomes. The nonprotein coding property verified. Various vitro vivo experiments were performed interaction between YAP signaling.We that is overexpressed PDAC multiple...
Abstract Atherosclerosis is a chronic inflammatory disease caused mainly by lipid accumulation and excessive immune response. Although the lipid-lowering cardioprotective properties of bilirubin, as well negative relationship between bilirubin atherosclerosis, were documented, it not yet clear whether can attenuate atherosclerosis in vivo. In this study, we investigated role improving atherosclerosis. We found that mildly elevated significantly reduced risk factors such plasma glucose, total...
Hepatocellular carcinoma (HCC), the most common type of primary liver cancer, remains a global health challenge requiring novel and effective therapeutic agents approaches. Here, we found that natural product plumbagin can inhibit growth HCC cells by inducing downregulation GPX4, but not other antioxidant enzymes such as CAT, SOD1, TXN. Functionally, genetic silence GPX4 enhances, whereas overexpression inhibits plumbagin-induced apoptosis (rather than ferroptosis) in cells. Furthermore,...
Background: Chemoresistance is a significant obstacle to the effective treatment of breast cancer (BC), resulting in more aggressive behavior and worse clinical outcome.The molecular mechanisms underlying chemoresistance remain unclear.Our microarray analysis had identified overexpression small glycoprotein serglycin (SRGN) multidrug-resistant BC cells.Here, we aimed investigate role SRGN elucidate mechanisms.Methods: SRNG was using its relevance analyzed.To SRGN, performed various vitro...
Abstract Background Hepatocellular carcinoma (HCC) remains a medical challenge due to its high proliferation and metastasis. Although deubiquitinating enzymes (DUBs) play key role in regulating protein degradation, their pathological roles HCC have not been fully elucidated. Methods By using biomass spectrometry, co-immunoprecipitation, western blotting immunofluorescence assays, we identify ribosomal S16 (RPS16) as substrate of ubiquitin-specific peptidase 1 (USP1). The USP1-RPS16 axis the...
Abstract N6-methyladenosine (m 6 A) modification plays important roles in bioprocesses and diseases. AlkB homolog 5 (ALKBH5) is one of two m A demethylases. Here, we reveal that ALKBH5 acetylated at lysine 235 (K235) by acetyltransferase 8 deacetylated histone deacetylase 7. K235 acetylation strengthens the demethylation activity increasing its recognition on mRNA. RNA-binding protein paraspeckle component 1 (PSCP1) a regulatory subunit preferentially interacts with K235-acetylated to...
// Hongbiao Huang 1, * , Yuning Liao Ningning Liu 2 Xianliang Hua 1 Jianyu Cai Changshan Yang Huidan Long Chong Zhao Xin Chen Xiaoying Lan Dan Zang Jinjie Wu Xiaofen Li Xianping Shi Xuejun Wang 3 Jinbao State Key Laboratory of Respiratory Disease, Protein Modification and Degradation Laboratory, Department Pathophysiology, Guangzhou Medical University, Guangdong 511436, People’s Republic China Research Institute Cardiovascular The Second Affiliated Hospital, 510260, Division Basic...