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Crosstalk between ferroptosis and stress—Implications in cancer therapeutic responses

Cancer Innovation 2022年第1期1卷 92-113页

作者： Cheng Zhang Jiao‐jiao Yu Chen Yang Shuang Shang Xiao‐xi Lv Bing Cui Fang Hua CAMS Key Laboratory of Molecular Mechanism and Target Discovery of Metabolic Disorder and Tumorigenesis State Key Laboratory of Bioactive Substance and Function of Natural MedicinesInstitute of Materia MedicaChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijingChina

Ferroptosis is a newly discovered form of cell death that is characterized by the accumulation of iron‐dependent lipid peroxidation.Research on ferroptosis has seen exponential growth over the past few years.Tumor cells are strongly dependent on iron for their growth,which makes them develop mechanisms to increase iron uptake and inhibit iron output,thereby completing iron accumulation.Ferroptosis can be induced or inhibited by various stresses through multiple mechanisms,making it stands at the crossroads of stresses related cancer cell fate determination.In this review,we give a brief summary of ferroptosis hallmarks and provide a systematic analysis of the current molecular mechanisms and regulatory networks of diverse stress conditions on ferroptosis.We also discuss the relationships between ferroptosis and cancer therapy responses to further understand potential targets and therapeutic strategies for cancer treatment.

关键词： tumor therapeutic response ferroptosis stress crosstalk

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Protein acylation:mechanisms,biological functions and therapeutic targets

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Signal Transduction and targeted Therapy 2023年第1期8卷 220-249页

作者： Shuang Shang Jing Liu Fang Hua CAMS Key Laboratory of Molecular Mechanism and Target Discovery of Metabolic Disorder and Tumorigenesis State Key Laboratory of Bioactive Substance and Function of Natural MedicinesInstitute of Materia MedicaChinese Academy of Medical Sciences&Peking Union Medical College100050 BeijingP.R.China

metabolic reprogramming is involved in the pathogenesis of not only cancers but also neurodegenerative diseases,cardiovascular diseases,and infectious diseases.With the progress of metabonomics and proteomics,metabolites have been found to affect protein acylations through providing acyl groups or changing the activities of acyltransferases or deacylases.Reciprocally,protein acylation is involved in key cellular processes relevant to physiology and diseases,such as protein stability,protein subcellular localization,enzyme activity,transcriptional activity,protein–protein interactions and protein–DNA interactions.Herein,we summarize the functional diversity and mechanisms of eight kinds of nonhistone protein acylations in the physiological processes and progression of several diseases.We also highlight the recent progress in the development of inhibitors for acyltransferase,deacylase,and acylation reader proteins for their potential applications in drug discovery.

关键词： diseases cardiovascular mechanisms

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TRIB3-GSK-3β interaction promotes lung fibrosis and serves as a potential therapeutic target

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Acta Pharmaceutica Sinica B 2021年第10期11卷 3105-3119页

作者： Shanshan Liu Xiaoxi Lv Xupeng Wei Chang Liu Qiao Li Jiali Min Fang Hua Xiaowei Zhang Ke Li Pingping Li Yang Xiao Zhuowei Hu Bing Cui State key laboratory of Bioactive Substance and Function of Natural Medicines Institute of Materia MedicaCAMS Key Laboratory of Molecular Mechanism and Target Discovery of Metabolic Disorder and TumorigenesisChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100050China Department of Pharmacy Pharmacy CollegeHebei UniversityBaoding 071000China National Clinical Research Center for metabolic Diseases Department of Metabolism and Endocrinologythe Second Xiangya HospitalCentral South UniversityChangsha 410011China Institute of Medicinal Biotechnology Chinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100050China

Pulmonary fibrosis(PF)is a chronic,progressive,fatal interstitial lung disease with limited available therapeutic strategies.We recently reported that the protein kinase glycogen synthase kinase-3β(GSK-3β)interacts with and inactivates the ubiquitin-editing enzyme A20 to suppress the degradation of the transcription factor CCAAT/enhancer-binding protein beta(C/EBPβ)in alveolar macrophages(AMs),resulting in a profibrotic phenotype of AMs and promoting the development of PF.Here,we showed that chronic lung injury upregulated the stress response protein tribbles homolog 3(TRIB3),which interacted with GSK-3βand stabilized GSK-3βfrom ubiquitination and degradation.Elevated GSK-3βexpression phosphorylated A20 to inhibit its ubiquitin-editing activity,causing the accumulation of C/EBPβand the production of several profibrotic factors in AMs and promoting PF development.Activated C/EBPβ,in turn,increased the transcription of TRIB3 and GSK-3β,thereby establishing a positive feedback loop in AMs.The knockdown of TRIB3 expression or the pharmacologic disruption of the TRIB3-GSK-3βinteraction was an effective PF treatment.Our study reveals an intact profibrotic axis of TRIB3-GSK-3β-A20-C/EBPβin AMs,which represents a target that may provide a promising treatment strategy for PF.

关键词： E3 ligase Lung injury Protein phosphorylation Protein-protein interaction Ubiquitination TRIB3 GSK-3β

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