Evidence map›Paper›PMID 41177429›Full record

ArticleJournal of advanced research2026

IDR-driven LLPS of GAS2L3 scaffolds CHMP4B condensates to accelerate cytokinesis in hepatocellular carcinoma cells.

Yan Zhao, Miao Zheng, Peiying Li, Chunyan Zhao, Rui Chen, Baoxin Qian, Xiaoteng Cui, Yuanyuan Ren, Chao Su, Lei Shi and 4 more

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Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

14 authors.

Yan ZhaoState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China.
Miao ZhengState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China.
Peiying LiState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China.
Chunyan ZhaoState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China; Department of Medical Laboratory, Tianjin Hospital, Tianjin University, Tianjin, China.
Rui ChenState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China.
Baoxin QianState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China; Department of Gastroenterology and Hepatology, Tianjin Third Central Hospital / Central Hospital, Tianjin University, Tianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Tianjin Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, Tianjin, China.
Xiaoteng CuiState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China; Laboratory of Neuro-oncology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Yuanyuan RenState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China.
Chao SuDivision of Cardiac Surgery, Cardiovascular Medical Center, the University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Lei ShiState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China.
Jihui HaoDepartment of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin' s Clinical Research Center for Cancer, Tianjin, China.
Zhi YaoState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China.
Xingjie GaoState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China. Electronic address: gaoxingjie@tmu.edu.cn.
Jie YangState Key Laboratory of Experimental Hematology, Key Laboratory of Cellular and Molecular Immunology in Tianjin, and Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Science, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Medical University, Tianjin, China; Department of Biochemistry and Molecular Biology, Department of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China. Electronic address: yangj@tmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDysregulated cell cycle progression is a hallmark of cancer, promoting uncontrolled cell proliferation. Growth arrest-specific 2 like 3 (GAS2L3), which is highly expressed in hepatocellular carcinoma (HCC) cells, correlates with poor clinical outcomes. However, the role of GAS2L3 in HCC pathogenesis remains unclear.

objectivesThis study aimed to investigate the molecular mechanisms by which GAS2L3 contributes to cytokinesis and hyperproliferation of HCC cells.

methodsLoss-of-function assays of GAS2L3 were performed to assess midbody assembly, a process essential for cytokinesis. By analyzing protein structure, we predicted liquid-liquid phase separation (LLPS) potential of GAS2L3, which was validated via fluorescence recovery after photobleaching (FRAP), time-lapse imaging, and in vitro droplet formation assays. Additionally, we generated an intrinsically disordered region (IDR)-deficient model to investigate the role of IDR in LLPS and its effects on cytokinesis, cell cycle progression, and HCC tumorigenicity.

resultsHighly expressed GAS2L3 localizes to the midbody and accelerates the cytokinesis of HCC cells by facilitating the recruitment of the charged multivesicular body protein 4B (CHMP4B). Notably, EGFP-GAS2L3 aggregates in the midbody exhibit dynamic behavior. Structural analysis and experimental evidence confirm GAS2L3 undergoes phase separation via its IDR. GAS2L3 scaffolds the CHMP4B condensate formation at midbody through phase separation, thereby accelerating cytokinesis in HCC cells. Moreover, GAS2L3 knockdown or IDR deletion in HCC cells leads to defective cytokinesis, G1 arrest, and significant tumorigenicity inhibition.

conclusionGAS2L3 critically regulates cytokinesis in HCC through LLPS-mediated remodeling of midbody abscission microenvironment. These findings reveal novel insights into HCC hyperproliferation and suggest GAS2L3 as a potential therapeutic target.

Indexed as

Carcinoma, HepatocellularCytokinesisEndosomal Sorting Complexes Required for TransportLiver NeoplasmsAnimalsCell Line, TumorCell ProliferationHumansMicePhase SeparationCHMP4B protein, humanEndosomal Sorting Complexes Required for TransportCytokinesisGAS2L3HCCLLPSMidbodyProliferation

Identifiers

PMID41177429
PMCPMC13316498

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