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Ca2+ transmembrane transport enhances oscillatory growth of cancer cell invadopodia

文献类型：期刊论文

作者Zhao, Junbo2; Zhang HC(张颢辰)1; Yang, Yuehua2; Xue, Ruihao2; Gong, Ze2,3; Jiang, Hongyuan2
刊名COMMUNICATIONS PHYSICS
出版日期2025-08-23
卷号8期号:1页码:10
ISSN号2399-3650
DOI10.1038/s42005-025-02268-x
通讯作者Gong, Ze(gongze@ustc.edu.cn) ; Jiang, Hongyuan(jianghy@ustc.edu.cn)
英文摘要Invadopodia, dynamic cancer cell protrusions, deform and degrade extracellular matrix (ECM) to facilitate invasion. Intracellular calcium ions (Ca2+) are critical second messengers involved in cancer cells migration, proliferation, and apoptosis, but their role in invadopodia dynamics remains unclear. Here, we propose a chemo-mechanical model integrating Ca2+ transmembrane transport, myosin contractility, adhesion dynamics, actin polymerization, and membrane type 1 matrix metalloproteinase (MT1-MMP) hydrolysis. We find that increased invadopodia length elevates membrane tension, activating mechanosensitive channels and raising intracellular Ca2+ levels, aligning with experimental observations. Our model reveals that invadopodia oscillatory and monotonic dynamics are governed by actin polymerization and myosin recruitment, with Ca2+ transport enhancing dynamics via myosin recruitment and reciprocal effects on Ca2+ transport. Furthermore, by incorporating MT1-MMP-mediated ECM degradation in our model, we find that ECM degradation promotes invadopodia extension and elevates Ca2+ levels, which shifts the invadopodia dynamics from monotonic to oscillatory. Overall, our model offers a comprehensive theoretical framework for understanding Ca2+ transport and invadopodia dynamics in cancer cells.
分类号二类/Q1
WOS关键词VOLUME REGULATION ; CALCIUM-CHANNELS ; EPITHELIAL-CELLS ; CATION CHANNEL ; TUMOR-CELLS ; MYOSIN-II ; EXPRESSION ; MIGRATION ; CORTACTIN ; STIFFNESS
资助项目National Natural Science Foundation of China (National Science Foundation of China)[12472323] ; National Natural Science Foundation of China (National Science Foundation of China)[12202439] ; National Natural Science Foundation of China (National Science Foundation of China)[12025207] ; National Natural Science Foundation of China (National Science Foundation of China)[11872357] ; National Natural Science Foundation of China[XDB1150000] ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Fundamental Research Funds for the Central Universities ; University of Science and Technology of China Center for Micro and Nanoscale Research and Fabrication
WOS研究方向Physics
语种英语
WOS记录号WOS:001556352000001
资助机构National Natural Science Foundation of China (National Science Foundation of China) ; National Natural Science Foundation of China ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Fundamental Research Funds for the Central Universities ; University of Science and Technology of China Center for Micro and Nanoscale Research and Fabrication
其他责任者Gong, Ze ; Jiang, Hongyuan
源URL[http://dspace.imech.ac.cn/handle/311007/103801]  
专题力学研究所_非线性力学国家重点实验室
作者单位1.Capital Med Univ, Sch Basic Med Sci, Dept Neurobiol, Beijing, Peoples R China;
2.Univ Sci & Technol China, Dept Modern Mech, CAS Key Lab Mech Behav & Design Mat, Hefei, Anhui, Peoples R China;
3.Chinese Acad Sci, Inst Mech, State Key Lab Nonlinear Mech, Beijing, Peoples R China
推荐引用方式
GB/T 7714		 Zhao, Junbo,Zhang HC,Yang, Yuehua,et al. Ca2+ transmembrane transport enhances oscillatory growth of cancer cell invadopodia[J]. COMMUNICATIONS PHYSICS,2025,8(1):10.
APA Zhao, Junbo,张颢辰,Yang, Yuehua,Xue, Ruihao,Gong, Ze,&Jiang, Hongyuan.(2025).Ca2+ transmembrane transport enhances oscillatory growth of cancer cell invadopodia.COMMUNICATIONS PHYSICS,8(1),10.
MLA Zhao, Junbo,et al."Ca2+ transmembrane transport enhances oscillatory growth of cancer cell invadopodia".COMMUNICATIONS PHYSICS 8.1(2025):10.

入库方式： OAI收割

来源：力学研究所

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