ArticleScience advances2021
The deacetylation-phosphorylation regulation of SIRT2-SMC1A axis as a mechanism of antimitotic catastrophe in early tumorigenesis.
Open access · goldAbstract read
In one paragraph
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- SMC1A is required for fate determinations of human spermatogonial stem cells and male fertility by interacting with YBX1 and stabilizing HMGA2 mRNA via an mCell death and differentiation · 2026Article
- Master Regulator SMC1A, Stabilized by N6-Methyladenosine Reader IGF2BP1, Promotes HCC Progression Through Facilitating Enhancer-Promoter Interaction of Nestin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multiple Regulatory Mechanisms of Post-Translational Modifications and Therapeutic Potential of Mitotic Catastrophe.International journal of molecular sciences · 2026Review
- The Sirt2-Nur77 axis regulates muscle stem cell quiescence and senescence via epigenetic-metabolic synergy.Cell death & disease · 2026Article
- Current Computational Approaches for the Discovery of Novel Anticancer Agents Targeting VEGFR and SIRT Signaling Pathways.Pharmaceutics · 2026Review
- A Novel MICB-Targeting CAR-NK Cells for the Treatment of Pancreatic Cancer.International journal of molecular sciences · 2026Article
- Meiotic cohesion requires Sirt1 and preserving its activity in aging oocytes reduces missegregation.EMBO reports · 2025Article
- An In Vivo Drug Screen Reveals That Sirtuin 2 Activity Promotes Spinal Cord Neurogenesis in Developing Zebrafish.Biomolecules · 2025Article
- GCLC desuccinylation regulated by oxidative stress protects human cancer cells from ferroptosis.Cell death and differentiation · 2025Article
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- Crosstalk between O-GlcNAcylation and ubiquitination: a novel strategy for overcoming cancer therapeutic resistance.Experimental hematology & oncology · 2024Review
- Targeting SIRT2 in Aging-Associated Fibrosis Pathophysiology.Aging and disease · 2024Review
- Unraveling the nexus between cellular senescence and malignant transformation: a paradigm shift in cancer research.Cancer biology & medicine · 2024Article
- SIRT2 promotes base excision repair by transcriptionally activating OGG1 in an ATM/ATR-dependent manner.Nucleic acids research · 2024Article
- Precisely modulating the chromatin trackerChemical science · 2024Article
- FBXO31 is upregulated by METTL3 to promote pancreatic cancer progression via regulating SIRT2 ubiquitination and degradation.Cell death & disease · 2024Article
- Structure, functions, and recent advances in the development of SIRT2 inhibitors.Pharmaceutical science advances · 2023Review
- RIT1 regulates mitosis and promotes proliferation by interacting with SMC3 and PDS5 in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- Regulation of RB1CC1/FIP200 stability and autophagy function by CREBBP-mediated acetylation in an intrinsically disordered region.Autophagy · 2023Article
- Oxidative stress impairs the Nur77-Sirt1 axis resulting in a decline in organism homeostasis during aging.Aging cell · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
31 authors at 8 institutions in 3 countries.
Fei YiInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.ORCID 0000-0002-4377-6285
Ying ZhangDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, China.ORCID 0000-0002-1961-899X
Zhijun WangInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.ORCID 0000-0002-5680-5006
Zhuo WangInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Ziwei LiInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Tingting ZhouInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Hongde XuInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.ORCID 0000-0002-8026-2443
Jingwei LiuInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Bo JiangInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Xiaoman LiInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Liang WangDepartment of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning Province 110122, China.
Ning BaiInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Qiqiang GuoInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Yi GuanInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.ORCID 0000-0002-1944-1610
Yanling FengInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.
Zhiyong MaoClinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200082, China.
Guangjian FanInstitute of Translational Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China.ORCID 0000-0003-0684-1380
Shengping ZhangInstitute of Translational Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China.ORCID 0000-0003-4088-2768
Chuangui WangInstitute of Translational Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China.
Longyue CaoWilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Brian P O'RourkeDepartment of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Yang WangPanjin Liaohe Oilfield Gem Flower Hospital, Panjin, Liaoning Province 124010, China.
Yanmei WuPanjin Liaohe Oilfield Gem Flower Hospital, Panjin, Liaoning Province 124010, China.
Boquan WuDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, China.
Shilong YouDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, China.
Naijin ZhangDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, China.ORCID 0000-0003-3653-9801
Junlin GuanDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.ORCID 0000-0001-8720-8338
Xiaoyu SongInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China. xysong@cmu.edu.cn yxsun@cmu.edu.cn swei@uabmc.edu lcao@cmu.edu.cn.ORCID 0000-0002-6606-327X
Yingxian SunDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, China. xysong@cmu.edu.cn yxsun@cmu.edu.cn swei@uabmc.edu lcao@cmu.edu.cn.ORCID 0000-0002-1961-899X
Shi WeiDepartment of Pathology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35249-7331, USA. xysong@cmu.edu.cn yxsun@cmu.edu.cn swei@uabmc.edu lcao@cmu.edu.cn.ORCID 0000-0003-4417-593X
Liu CaoInstitute of Translational Medicine, Key Laboratory of Cell Biology of Ministry of Public Health, and Key Laboratory of Medical Cell Biology of Ministry of Education, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, China Medical University, , No. 77, Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China. xysong@cmu.edu.cn yxsun@cmu.edu.cn swei@uabmc.edu lcao@cmu.edu.cn.ORCID 0000-0001-6471-1993
Ministry of Education · KRAlbert Einstein College of Medicine · USFirst Hospital of China Medical University · CNShanghai Jiao Tong University · CNUniversity of Alabama at Birmingham · USChina Medical University · CNSecond Hospital of Liaohe Oilfield · CNShanghai First Maternity and Infant Hospital · CN
Funding
No grant is acknowledged in the PubMed record.
Abstract
Improper distribution of chromosomes during mitosis can contribute to malignant transformation. Higher eukaryotes have evolved a mitotic catastrophe mechanism for eliminating mitosis-incompetent cells; however, the signaling cascade and its epigenetic regulation are poorly understood. Our analyses of human cancerous tissue revealed that the NAD-dependent deacetylase SIRT2 is up-regulated in early-stage carcinomas of various organs. Mass spectrometry analysis revealed that SIRT2 interacts with and deacetylates the structural maintenance of chromosomes protein 1 (SMC1A), which then promotes SMC1A phosphorylation to properly drive mitosis. We have further demonstrated that inhibition of SIRT2 activity or continuously increasing SMC1A-K579 acetylation causes abnormal chromosome segregation, which, in turn, induces mitotic catastrophe in cancer cells and enhances their vulnerability to chemotherapeutic agents. These findings suggest that regulation of the SIRT2-SMC1A axis through deacetylation-phosphorylation permits escape from mitotic catastrophe, thus allowing early precursor lesions to overcome oncogenic stress.
Indexed as
Antimitotic AgentsSirtuin 2AcetylationCarcinogenesisCell Cycle ProteinsChromosomal Proteins, Non-HistoneEpigenesis, GeneticHumansPhosphorylationStructural Maintenance of Chromosome Protein 1Antimitotic AgentsCell Cycle ProteinsChromosomal Proteins, Non-HistoneSIRT2 protein, humanSirtuin 2Structural Maintenance of Chromosome Protein 1
Identifiers
What OpenQuestion holds
Textmetadata
LicenceCC BY-NC
Read underepoch 390
Registered trials
None linked
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.